Week 3 Flashcards

1
Q

a localized dilation or outpouching of a vessel wall or cardiac chamber.

A

aneursym

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2
Q

True aneurysms

A

involve all three layers of the arterial wall and are best described as a weakening of the vessel wall. Most are fusiform and circumferential.

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3
Q

False aneurysm

A

is an extravascular hematoma that communicates with the intravascular space.

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4
Q

Arteriosclerosis and hypertension are found in more than half of all individuals with aneurysms.

A

Arteriosclerosis and hypertension are found in more than half of all individuals with aneurysms.

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5
Q

Aneurysms most commonly occur in the

A

thoracic or abdominal aorta.
-aorta has constant stress/pressure
-absence of penetrating vasa vasorum in the media layer.

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6
Q

Aortic Dissection

A

-devastating complication that can involve any part of the aorta (ascending, arch, or descending)
-can disrupt flow through arterial branches, thus creating a surgical emergency
-40% of patients die immediately from complete rupture and bleeding out from the aorta
-Sudden severe, sharp pain in chest or upper back; also described as a tearing, stabbing or ripping feeling, Shortness of breath, Fainting or dizziness, Low blood pressure; high suspicion when there’s a 20 mmHg pressure difference between arm

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7
Q

Ventricular Wall Aneurysm

A

-when intraventicular tensions stretches the non contracting infarcted muscle
-usually after heart attack
-With time the aneurysm becomes more fibrotic but continues to bulge with each systole, thus acting as a“reservoir”for some of the stroke volume.

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8
Q

Cerebral aneurysms are usually silent over their lifetime, but they sometimes can be complicated by subarachnoid hemorrhage

A

Cerebral aneurysms are usually silent over their lifetime, but they sometimes can be complicated by subarachnoid hemorrhage

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9
Q

diagnosis of an aneurysm

A

ultrasonography (US), CT, MRI, or angiography.

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10
Q

aneurysm treatment

A
  • maintain a low blood volume and low blood pressure to decrease mechanical forces
    -smoking cessation, reducing blood pressure and blood volume, and β-adrenergic blockage (beta-blockers).
    -Surgery when aortic aneurysms reach 5 cm in diameter
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11
Q

are men or women more effected by varicose veins

A

women

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12
Q

a superficial vein in which blood has pooled

A

various veinbs

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13
Q

varicose veins involve what veing

A

saphaneous

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14
Q

Varicose veins are caused by

A

-trauma to the saphenous veins that damages one or more valves
- gradual venous distention caused by the action of gravity on blood in the legs.

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15
Q

Damaged valves cannot maintain normal venous pressure, which causes hydrostatic pressure in the vein to increase. As the vein distends further, it becomes tortuous, and edema develops in the extremity.

A

Damaged valves cannot maintain normal venous pressure, which causes hydrostatic pressure in the vein to increase. As the vein distends further, it becomes tortuous, and edema develops in the extremity.

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16
Q

aricose veins can progress to

A

chronic venous insufficiency (CVI)

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17
Q

sustained inadequate venous return

A

chronic venous insufficiency (CVI)
-Venous hypertension, circulatory stasis, and tissue hypoxia lead to an inflammatory reaction in vessels and tissue. T

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18
Q

chronic venous insufficiency sxs

A

edema of the lower extremities
hyperpigmentation of the skin of the feet and ankles
sluggish metabloism to legs
Any trauma or pressure can therefore lower the oxygen supply and cause cell death and necrosis (venous stasis ulcers).

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19
Q

Treatment of Varicose Veins

A

leg elevation, compression stockings, and physical exercise.

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20
Q

A thrombus is a blood clot that remains attached to a vessel wall. A detached
thrombus is a thromboembolus.

A

A thrombus is a blood clot that remains attached to a vessel wall. A detached
thrombus is a thromboembolus.

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21
Q

Venous thrombi are more common than arterial thrombi because flow and pressure are lower in the veins than in the arteries.

A

Venous thrombi are more common than arterial thrombi because flow and pressure are lower in the veins than in the arteries.

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22
Q

clot formation in the large veins, primarily of the lower extremities and may result in venous thromboembolism (VTE) to the pulmonary circulation.

A

DVT

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23
Q

Causes of DVT

A
  1. Venous stasis (immobility, obesity, prolonged leg dependency [e.g., air travel], age, heart failure [HF])
  2. Vein endothelial damage (trauma medicine)
  3. Hypercoaguable states (e.g., inherited disorders, malignancy, pregnancy, oral contraceptives, hormone replacement, hyperhomocysteinemia, antiphospholipid syndrome).
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24
Q

Virtually everyone who is hospitalized is at significant risk for DVT,

A

Virtually everyone who is hospitalized is at significant risk for DVT,

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25
Q

does DVT have symptoms

A

no not usually cause the vein is deep

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26
Q

DVT sxs

A

-edema
-throbbing or cramping pain in 1 leg (rarely both legs), usually in the calf or thigh
-swelling in 1 leg (rarely both legs)
-warm skin around the painful area
-red or darkened skin around the painful area
-swollen veins (hard/sore)

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27
Q

Diagnosis of DVT

A

measurement of serum d-dimer
concentration with lower extremity ultrasound

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28
Q

D-dimer

A

protein fragment that your body makes when a blood clot dissolves in your body.

29
Q

Untreated DVT is associated with

A

pulmonary embolism

30
Q

Prevention/Treatment of DVT

A

-individuals should be mobilized as soon as possible after illness, injury, or surgery.
-heparin, antithrombin agents, warfarin, or pneumatic devices

31
Q

In the arteries, activation of the coagulation cascade usually is caused by roughening of the tunica intima by

A

atherosclerosis.

32
Q

Complications of Arterial Thrombus

A

1- thrombus may grow large enough to occlude the artery, causing ischemia in tissue supplied by the artery.
2) the thrombus may dislodge

33
Q

Diagnosis and treatment of arterial thrombi

A

Doppler ultrasonography and angiography
-heparin, warfarin derivatives, thrombin inhibitors, or thrombolytics

34
Q

the obstruction of a vessel by an embolus—a bolus of matter that is circulating in the bloodstream

A

embolism

35
Q

what can an embolism be

A

-dislodged thrombus
-an air bubble
-amniotic fluid
-aggregate of fat, bacteria, or cancer cells
-foreign substance.

36
Q

An embolus travels in the bloodstream until it reaches a vessel through which it cannot fit. No matter how tiny it is, an embolus eventually will lodge in a systemic or pulmonary vessel.

A

An embolus travels in the bloodstream until it reaches a vessel through which it cannot fit. No matter how tiny it is, an embolus eventually will lodge in a systemic or pulmonary vessel.

37
Q

Pulmonary emboli originate in the ___________(mostly from the deep veins of the legs) or in the right heart

A

venous circulation

38
Q

Arterial emboli most commonly originate in the

A

left heart

39
Q

Embolism causes ischemia or infarction in tissues distal to the obstruction. A limb that is ischemic because of arterial occlusion is characterized (1) by an almost waxy whiteness of the skin because the vasculature is devoid of erythrocytes, and (2) by numbness and pain resulting from neural ischemia.

A

Embolism causes ischemia or infarction in tissues distal to the obstruction. A limb that is ischemic because of arterial occlusion is characterized (1) by an almost waxy whiteness of the skin because the vasculature is devoid of erythrocytes, and (2) by numbness and pain resulting from neural ischemia.

40
Q

Embolism to a coronary or cerebral artery is an immediate threat to life if the embolus severely obstructs a major vessel.
Occlusion of a coronary artery causes an MI, whereas occlusion of a cerebral artery causes a stroke.

A

Embolism to a coronary or cerebral artery is an immediate threat to life if the embolus severely obstructs a major vessel.
Occlusion of a coronary artery causes an MI, whereas occlusion of a cerebral artery causes a stroke.

41
Q

Thickening and hardening of the vessel caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a plaque.

A

Atherosclerosis

42
Q

leading cause of coronary artery disease and cerebrovascular disease.

A

Atherosclerosis

43
Q

Atherosclerosis is an inflammatory disease that develops and proceeds in the presence of elevated

A

plasma cholesterol levels

44
Q

The lesions progress from

A

endothelial injury and dysfunction to
fatty streak to
fibrotic plaque to
complicated lesion

45
Q

risk factors for atherosclerosis

A

smoking, hypertension, diabetes, increased levels of low-density lipoprotein (LDL), decreased levels of high-density lipoprotein (HDL), and autoimmunity

-elevated homocysteine, C-reactive protein (CRP), increased serum fibrinogen, infection, and periodontal disease.

46
Q

Steps of atherloclerosis

A
  1. Injured endothelial cells become inflamed
  2. Numerous inflammatory cytokines are released, including tumor necrosis factor-alpha (TNF-α), interferon gamma (IFN-γ), interleukin-1 (IL-1), toxic oxygen radicals, CRP, and heat shock proteins. (free radicals)
  3. Macrophages adhere to injured endothelium
  4. macrophages release enzymes and toxic oxygen radicals that create oxidative stress, oxidize LDL, and further injure the vessel wall.
  5. Growth factors also are released, including angiotensin II, fibroblast growth factor, TGF-β, and platelet-derived growth factor, which stimulate smooth muscle cell proliferation in the affected vessel.
47
Q

what causes LDL to be oxidized

A

Inflammation, oxidative stress, and activation of macrophages

48
Q

___________ is toxic to endothelial cells and causes smooth muscle proliferation

A

Oxidized LDL

49
Q

Macrophages filled with oxidized LDL

A

foam cells

50
Q

can be found in the walls of arteries of most people, even young children

A

fatty streak

51
Q

Plaques that have ruptured are called

A

complicated plaques

52
Q

atherosclerosis sxs

A

Partial vessel obstruction may lead to transient ischemic events, often associated with exercise or stress. Once the lesion becomes complicated, increasing obstruction with superimposed thrombosis may result in tissue infarction.

53
Q

Coronary Artery Disease (CAD) caused by atherosclerosis is THE major cause of

A

myocardial ischemia

54
Q

Atherosclerotic obstruction of the vessels supplying the brain is the major cause of

A

stroke.

55
Q

arterial bruits and evidence of decreased blood flow to tissues.

A

athlerosclerosis

56
Q

treatment atherlosclerossis

A

exercise, smoking cessation, and control of hypertension and diabetes when appropriate while reducing LDL cholesterol by diet or medications or both.

57
Q

Atherosclerotic disease of arteries that perfuse the limbs, especially the lower extremities

A

peripheral artery disease

58
Q

intermittent claudication.

A

Pain in limbs because they are not receiving blood in PAD (peripheral artery disease)

59
Q

most common cause of coronary artery obstruction is

A

atherlosclerosis

60
Q

Infarction (irreversible myocardial injury) constitutes the often-fatal event known as a

A

heart attack

61
Q

Risk Factors for CAD

A

1) Advanced age
(2) Male gender or women after menopause
(3) Family history
4) Genetics
5) AB blood type

62
Q

abnormal concentrations of serum lipoproteins

A

Dyslipidemia

63
Q

esponsible
for the delivery of cholesterol to the tissues

A

LDL

64
Q

cholesterol associated with CAD

A

high LDL
low HDL

65
Q

what cholesterol can also remove excess cholesterol from the arterial wall

A

HDL

66
Q

Troponin I (TnI) is a serum protein whose measurement is used as a sensitive and specific diagnostic test to help identify myocardial injury during acute coronary syndromes.

A

Troponin I (TnI)

67
Q

vitamins associated with homocysteine (help lower it)

A

folate
cobalamin (B12)
pyridoxine (B6)

68
Q

anti-inflammatory adipokine
-helps with insulin sensitivity and weight loss

A

adiponectin