Ch. 18 Disorders of Blood Flow and Blood Pressure Flashcards

1
Q

What are the 3 walls of blood vessels from outermost to innermost?

A
  1. Tunica Externa/Adventitia
  2. Tunica Media
  3. Tunica Intima
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2
Q

Describe the Tunica Externa

A
  • primarily loosely woven collagen fibers that protect the blood vessel and anchor it to the surrounding tissue
  • nerve fibers
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3
Q

Describe the Tunica Media

A

-mainly of circulatory arranged smooth muscle cells and sheets of elastin

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4
Q

describe the tunica intima

A

single layer of flattened endothelial cells with minimal underlying subendothelial connective tissue

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5
Q

What does the endothelium of blood vessels do?

A
  • versatile, lots of functions
  • selective permeability (inflammatory response)
  • helps modulate blood flow
  • vascular resistance (dilate/constrict)
  • helps with platelet adhesion
  • regulates inflammatory actions
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6
Q

What are some dysfunctions that can occur with the endothelium of blood vessels?

A
  • thrombus formation w/o injury
  • atherosclerosis
  • Hypersensitive vascular lesions
  • erectile dysfunction
  • retina disorders
  • kidney disorders
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7
Q

Arteries, arterioles, capillaries

A

arteries: main transporters of oxygenated blood
arterioles: diameter is adjusted to regulate blood flow
capillaries: diffusion occurs across thin walls

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8
Q

give examples of large, medium, and small arteries

A

large: aorta
medium: coronary and renal
small: arteries and arterioles

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9
Q

Hyperlipidemia/Hyperlipoproteinemia

A

increased lipids in the blood

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10
Q

describe the pathology behind hyperlipidemia

A

-because lipids, namely cholesterol and triglycerides, are insoluble in plasma, they are encapsulated by special fat carrying proteins called lipoproteins for transport in the blood.

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11
Q

what are the 5 types of lipoproteins?

A
  • chylomicrons
  • Very-low density lipoprotein (VLDL)
  • intermediate-density lipoprotein (IDL)
  • low-density lipoprotein (LDL)
  • high-density lipoprotein (HDL)
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12
Q

how are lipoproteins classified?

A

based on their density

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13
Q

chylomicrons

A

lowest density

  • 80-90% triglycerides
  • 2% protein
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14
Q

VLDL

A
  • converted to LDL in the body
  • 65% triglycerides
  • 10% cholesterol
  • 5-10% protein
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15
Q

LDL

A
  • “bad cholesterol”
  • main carrier of cholesterol; 50% cholesterol
  • 10% triglycerides
  • 25% protein
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16
Q

HDL

A
  • “good/healthy cholesterol”
  • 5% triglycerides
  • 20% cholesterol
  • 50% protein
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17
Q

why is HDL considered “good cholesterol”?

A
  • it participates in reverse transport of cholesterol – that is, carrying cholesterol from the peripheral tissues back to the liver (to get rid of it)
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18
Q

Hypercholesteremia

A
  • increased levels of cholesterol in the blood
  • usually multifactorial
  • primary (develops independent of other causes) or secondary (associated with other health problems/behaviors)
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19
Q

What are some examples of causes of primary hypercholesteremia?

A
  • genetic base
  • defect in the synthesize of apoproteins
  • lack/deficiencies in receptors
  • defects in handling of cholesterol in the cell that are genetically determined
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20
Q

what are some examples of causes of secondary hypercholesteremia?

A
  • lifestyle causes
  • diet- high calorie intake
  • obesity (high triglycerides)
  • sedentary lifestyle
  • diabetes mellitus (high triglycerides)
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21
Q

how is hypercholesteremia diagnosed?

A

blood lipid studies

-could also be part of screening

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22
Q

how is hypercholesteremia managed?

A
  • goal is to decrease LDL( main carrier of cholesterol)
  • dietary changes; reduce calories, stay away from saturated fats (vegetable fats > animal fats)
  • stop smoking
  • medications: lipid lowering medications ( decrease cholesterol production, block cholesterol absorption, remove cholesterol from blood)
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23
Q

Atherosclerosis

A
  • hardening of the blood vessels
  • denotes the formation of fibrous fatty lesions in the intimal lining of the large and medium sized arteries (aorta, coronary arteries, cerebral arteries)
  • once plaques form, more elements stick to it and it can build up and form a blockage (risk of breaking off and going to organs)
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24
Q

Atherosclerosis is the leading cause of what?

A

coronary artery disease, stoke, and peripheral artery disease

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25
Q

what are some modifiable risk factors for atherosclerosis?

A

-smoking, obesity, HTN, salt intake, exercise, about on Hyperlipidemia, diabetic

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26
Q

what are some constitutional (unmodifiable) risk factors for atherosclerosis?

A
  • age, sex, genetics
  • family history
  • men age 45 and older
  • women age 55 and older or who experienced premature menopause with estrogen replacement
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27
Q

what are the three types of lesions associated with development of atherosclerosis?

A
  1. fatty streak
  2. fibrous atheromatous plaque
  3. complicated lesion
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28
Q

which two types of lesions are responsible for the clinically significant manifestations of atherosclerosis?

A
  • fibrous atheromatous plaque and complicated lesions
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29
Q

what are fatty streaks?

A
  • thin, flat, yellow, intimal discolorations that progressively enlarge by becoming thicker and slightly elevated as they grow in length
  • common within the first year of a child’s life (normal?)
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30
Q

what is the most important complication of atherosclerosis?

A

thrombosis

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31
Q

what are the stages of atherosclerosis development?

A
  1. endothelial cell injury (smoking, elevated LDL, HTN)
  2. migration of inflammatory cells- endothelial cells being to express selective adhesion molecules that bind monocytes. after monocytes adhere they migrate between the endothelial cells to localize in the intima, transform into macrophages and engulf lipoproteins (largely LDL)
  3. smooth muscle cell proliferation and lipid deposition- activated macrophages release toxic oxygen species that oxidize LDL resulting in the formation of FOAM CELLS. macrophages also produce growth factors that contribute to the migration and proliferation of smooth muscle cells.
  4. gradual development of the atheromatous plaque with a lipid core - cap forms over foam cells. the cap can erode, ulcerate, and break free
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32
Q

foam cells are the primary component of what vascular disease?

A

atherosclerosis

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33
Q

Clinical manifestations of atherosclerosis

A
  • depends on the vessels involved and the extent of vessel obstruction
  • carotid arteries can actually be cleaned out
  • coronary arteries,
  • aortic artery
  • legs
  • brain
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34
Q

Vasculitides

A
  • a group of vascular disorders that cause inflammatory injury and necrosis of the blood vessel wall (i.e. vasculitis) and necrosis of the blood vessel wall (vein capillary) .
  • vasculitis may result from direct injury to the vessel, infectious agents or immune processes or they may develop secondary to other disease states such as systemic lupus erythematosus
  • classified: small vessel, medium vessel, large vessel
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35
Q

what autoimmune disorder is associated with small vessel Vasculitides?

A

-scleroderma

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36
Q

what autoimmune disorder is associated with large vessel Vasculitides?

A

rheumatoid arthritis

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37
Q

what are the 3 types of arterial disease of the extremities?

A

peripheral arterial disease
Buerger disease
Raynaud’s Disease

38
Q

PAD: Peripheral Arterial Disease

A
  • aka: PVD
  • presence of systemic atherosclerosis distal to the arch of the aorta
  • commonly seen in vessels of the lower extremities; superficial femoral and popliteal
39
Q

who is PAD most commonly seen in?

A

men in there 60s and 70s

40
Q

what are some risk factors for PAD?

A
  • similar to those of atherosclerosis

- cigarette smoking, diabetes mellitus

41
Q

S/S of PAD

A
  • symptoms start when there is at least 50% occlusion of the vessel with related ischemia
  • primary symptom is calf pain/ intermittent claudication
  • regional pain that is worse at night but better when standing
  • atrophic changes, thinning of skin and subcutaneous tissues, muscle atrophy
  • cool foot, weak/absent popliteal and pedal pulses
  • limb color blanches with elevation
  • deep red when leg is in dependent position
  • tissue necrosis
42
Q

What is pain while walking called?

A

intermittent claudication

43
Q

how do you diagnose PAD?

A
  • inspection (loss of hair, brittle nails, pallor, dependent rubor)
  • palpation (femoral, popliteal, posterior tibial, dorsalis pedis)
  • blood pressures of legs
  • Doppler
  • ultrasound
  • angiography (injected dyes and take pictures)
44
Q

Treatment of PAD

A

-includes measures directed at protection of the affected tissues and preservation of functional capacity

  • increasing collateral circulation
  • avoidance of injury (injuries slow to heal)
  • addressing risk factors (smoking, HTN, diabetes)
  • medication (antiplatelet therapy - aspirin, vasodilators)
  • surgery
45
Q

Buerger Disease

A
  • aka: thromboangiitis obliterans
  • vasculitis affecting medium sized arteries
  • plantar and digital vessels in foot and lower leg
  • may affect the arms/hands
  • inflammatory process extends to involve adjacent veins and nerves

Risk factors: men age 25-40 who smoke, young female smokers,

S/S: pain, intermittent claudication (foot arch, digits), increase sensitivity to cold, extremities turn blue when person assumes a dependent position, shiny skin, lack of hair, thick malformed nails,

46
Q

Raynaud’s Disease

A
  • a phenomenon
  • the arteries and arterioles in fingers and less often toes are affected
  • intense vasospasm and inflammation
  • often some form of genetic link
47
Q

S/S of Raynaud’s of Disease

A
  • pain (b/c no profusion, nerves being affected)
  • temperature (feel cool, sensitive to cold)
  • color - cyanosis, pallor but after event the skin turns back red as the profusion returns
  • weak pulses
  • paresthesia (tingling) after event
48
Q

How to Diagnose Raynaud’s

A
  • History of vasospastic attacks
  • laser-Doppler
  • computed thermography (look at movement of heat)
49
Q

treatment of Raynaud’s

A
  • eliminating causes of vasospasms (wear gloves)
  • medication
  • surgery
50
Q

Aneurysm

A

an abnormal localized dilation of a blood vessel

-can occur in arteries and veins but most common in aorta

51
Q

True aneurysm

A
  • the aneurysm is bound by a complete vessel wall

- aneurysm remains in the vascular compartment

52
Q

false aneurysm

A
  • a localized dissection or tear in the inner wall of the artery with formation of an extravascular hematoma that causes vessel enlargement
  • bound only by the outer layers of the vessel wall or supporting tissues
53
Q

dissection

A

a tear

54
Q

what is the difference between a saccular aneurysm and a fusiform aneurysm?

A

a fusiform aneurysm involves the entire circumference of the vessel and is characterized by a gradual and progressive dilation of the vessel. A saccular aneurysm extends over part of the circumference of the vessels and appears saclike

55
Q

Dissecting aneurysm

A

a false aneurysm resulting from a tear in the intimal layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood filled cavity

56
Q

when do Abdominal Aortic Aneurysms usually occur and who does it most often affect?

A
  • after age 50

- men

57
Q

what is the major cause of abdominal aortic aneurysms?

A

-atherosclerosis

58
Q

where are abdominal aortic aneurysms usually located?

A
  • often located below level the renal artery, therefore they may first be noticed as a painless pulsating mass (DO NOT PALPATE)
  • can involve any part of the vessel : circumference (saccular) or extended to involve the entire circumference (fusiform)
59
Q

Diagnosis of Abdominal Aortic Aneurysms

A
  • ultrasound
  • echocardiography(camera dropped down esophagus)
  • CT scan
  • MRI
60
Q

Treatment of Abdominal Aortic Aneurysms

A
  • surgery
61
Q

what are the clinical manifestations of Aortic Dissection?

A
  • Syncope - feeling dizzy
  • Hemiplegia - cant move one side
  • pain
  • blood pressure and pulse rate become unobtainable in one or both arms
62
Q

Diagnosis of Aortic Dissections

A
  • history and physical
  • aortic angiography
  • transesophageal echocardiography
  • CT
  • MRI
63
Q

Treatment of Aortic Dissections

A
  • surgery
  • medical
  • placement of a stent (fake tubing)
64
Q

HTN

A
  • high blood pressure, hypertension

- often undiagnosed until complications with age

65
Q

Whose more likely to suffer from HTN?

A
  • men
  • African americans
  • incidence increased with age, often undiagnosed until complications with age
66
Q

Healthy BP

A

110/70, below 120/80 mmHg

67
Q

Prehypertension

A

120/80 to 139/89 mmHg

68
Q

Stage 1 HTN

A

140/90 to 159/99 mmHg

69
Q

Stage 2 HTN

A

160/100 mmHg

70
Q

a person is said to have HTN when..

A

BP is greater than 140/90

71
Q

is it worse to have a higher systolic or diastolic?

A

diastolic because this means that even when your heart is at rest there is a high amount of pressure. systolic refers to the pressure from the contraction of the heart

72
Q

Essential/Primary HTN

A
  • chronic elevation of BP occurs without evidence of other disease
  • account for 90% to 95% of HTN
73
Q

Secondary HTN

A

the elevation of blood pressure results from some other disorder

74
Q

Malignant HTN

A

sudden elevation of blood pressure

75
Q

untreated HTN is often called…

A

the silent killer

76
Q

HTN Manifestations

A

Worry about Target Organ Damage

  • Heart : left ventricular hypertrophy, angina, MI, Heart failure
  • Brain: stroke, TIA (transient ischemic attack)
  • CRF - Chronic Kidney Disease
  • PVD - Peripheral Vascular Disease
  • Retinopathy
77
Q

HTN Crisis

A

KNOW MARKERS…

  • Severe hypertension is systolic greater than 180 mmHg
  • Hypertensive urgency is an elevation in diastolic pressure great than 110 mmHg with symptoms
  • Hypertensive emergency is a diastolic greater than 120 mmHg resulting in end organ damage
78
Q

How do you know if someone has Sever Hypertension Crisis?

A

a systolic greater than 180 mmHg

79
Q

How do you know if someone is having a Hypertensive Urgency Crisis?

A

an elevation in diastolic pressure great than 110 mmHg with symptoms

80
Q

How do you know if someone is having a Hypertensive Emergency Crisis?

A

a diastolic greater than 120 mmHg resulting in end organ damage

81
Q

What is orthostatic HTN?

A
  • abnormal drop in blood pressure when assuming a standing position
  • 500-700 ml of blood is shifted to the lower part of the body
  • transient drop in blood pressure for several cardiac cycles
  • associated with dizziness and syncope
  • seen in older people, especially on anti-hypertension medication
  • could also be the result of dehydrations
82
Q

How do you diagnose Orthostatic HTN?

A
  • assess with obtaining blood pressure in different positions
    1. lying
    2. sitting
    3. standing

-does this person have a history of falling?

83
Q

Varicose Veins

A

-irregular dilated or tortuous areas of superficial or deep veins

84
Q

S/S of Varicose Veins

A
  • varicosities on the legs appear as irregular, purplish bulging structures
  • may be edema in the feet as venous pressure rises
  • fatigue and aching are common
  • shiny pigmented, hairless skin
  • varicose ulcers may develop as arterial blood flow continues to diminish and break down skin
85
Q

Treatment of varicose veins

A
  • surgical/cosmetic

- to prevent as well as treat wear compression hoes

86
Q

Thrombophlebitis (DVT)

A
  • development of a thrombus in a vein in which inflammation is present
  • platelets adhere to inflamed site and thrombus develops
  • seen in a lot of bed ridden patients, long car/plane rides, pregnancy
87
Q

Treatment of DVT

A

-anticoagulation therapy (heparin) and elevation of the affected leg

88
Q

Predisposing factors of DVT

A
  • stasis of blood or sluggish blood flow
  • endothelial injury-trauma, chemical injury, intravenous injection or inflammation
  • increased blood coagulability
89
Q

S/S DVT

A

-deep muscle pain at night, swollen/fluid build up, tender, increased warmth, discoloration

90
Q

A patient comes in with pain described as traveling straight through their abdomen, what do you expect that person is suffering from?

A

fusiform abdominal aortic aneurysm