Cardiovascular disease and atherosclerosis Flashcards

1
Q

Cardiovascular Disease

A

Defined by the presence of stenosis which impairs blood flow.
Flow limiting lesion.

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2
Q

Major Risk Factors for Cardiovascular Disease (non modifiable)

A
Gender (Male>Female)
Age
Male >40
Female >50 (post menopause)
Race (African American or Asian)
Family History
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3
Q

Major Risk Factors for Cardiovascular Disease (modifiable)

A
Hypertension
Tobacco use
Elevated blood glucose (IFG/diabetes)
Physical inactivity
overweight or obese
hyperlipidemia
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4
Q

Atherosclerosis

A

Commonly known as “hardening of the arteries.”

pathogenesis involves lipids, thrombosis, elements of the vascular wall, and immune cells.

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5
Q

Structure of Arterial Wall

A

intima: has endothelial cells
media: smooth muscle cells
adventia

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6
Q

Three Main Pathological Stages

A

Fatty Streak
Plaque Progression
Plaque Disruption

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7
Q

Fatty Streak

A

Endothelial dysfunction
Lipoprotein entry and modification
Leukocyte recruitment
Foam cell formation

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8
Q

Plaque Progression

A

smooth muscle cell migration

Altered matrix synthesis and degradation

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9
Q

Plaque Disruption

A

Disrupted plaque integrity

Thrombus formation

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10
Q

Role of Endothelial Cells (EC)

A

EC normally produce
antithrombotic molecules that prevent blood clots.
EC modulate the immune response
by resisting leukocyte adhesion and therefore inhibiting inflammation

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11
Q

Endothelial Dysfunction

A

↑ Permeability
↑ Inflammatory cytokines
↑ Leukocyte adhesion molecules
↓ Vasodilatory molecules

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12
Q

Lipoprotein Entry and Modification

A

↑ Permeability allows LDL entry
into the intima
LDL accumulate in the subendothelial space by binding to components of the extracellular matrix and become ‘trapped.’

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13
Q

Evolution of Atherosclerotic Plaque: developmental stage Fatty streaks

A

Characterized by lipid-filling smooth muscle cells

potentially reversible

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14
Q

Evolution of Atherosclerotic Plaque: developmental stage Fibrous plaque

A

Lipoproteins transport/deposits LDLs into the arterial intima

Fatty streak is covered by collagen and calcium deposits forming a fibrous plaque that appears grayish or whitish
resulting in narrowing of vessel

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15
Q

Evolution of Atherosclerotic Plaque: developmental stage Complicated lesion/Unstable Plaques

A

Continued inflammation can result in plaque instability, ulceration, and rupture.

Lipid core is exposed to the blood stream, platelets accumulate, and thrombus forms.

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16
Q

Complications of Atherosclerosis

A

acute coronary syndrome, myocardial infarction, Venous thromboembolism, stroke, Aneurysm, Hemorrhage

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17
Q

Peripheral Vascular Disease (PVD)

A

A slow and progressive circulation disorder caused by narrowing, blockage, or spasms in a blood vessel.
PVD may involve disease in any of the blood vessels outside of the heart
Arteries (PAD)
Veins (CVI)

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18
Q

Peripheral Arterial Disease causes

A

Structural changes in the vessel wall
Narrowing of the vascular lumen.
Spasm of vascular smooth muscle cell

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19
Q

Claudication Walking Tests

A

Measure distance the patient can ambulate before stopping due to claudication pain.
Claudication pain of PAD occurs at predictable and reproducible durations if exercise intensity is kept consistent.

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20
Q

Peripheral Arterial Disease Findings

A

Affected limb may show sings of cyanosis

Limbs may feel cool to the touch

Numbness or tingling reported in affected area

Skin may appear shiny, thin, pale, and hairless.

Nails become thickened and brittle.

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21
Q

Clinical Implications for PAD

A

Exercise at least 3 x/week
Initial workload/intensity should induce claudication within 3-5 min
Continues at this workload until the pain is of mod severity (5/10)

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22
Q

Raynaud’s Syndrome

A

Vasospasm causing reduced blood flow

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23
Q

Aneurysms

A

Localized abnormal dilation by at least 50% compared to normal.

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24
Q

Causes of aneurysms

A

atherosclerosis, congenital infections, Marfan’s

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25
Risk Factors aneurysms
``` Cardiovascular disease and Risk factors for CVD Especially smoking Male Genetics (Marfan’s) 40-60 yr old Hypertension prevalent ```
26
Types of Aneurysms
Saccular aka Berry Fusiform Dissecting
27
Saccular aka Berry Aneurysms
Small, spherical, 1-1.5 cm. | Most common in brain tissue
28
Fusiform Aneurysms
Gradual more progressive
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Dissecting Aneurysms
Blood filled channel within vessel wall
30
Abdominal Aortic Aneurysm symptoms
``` Dull, tearing ache/pain in low back, groin or mid abdominal left flank Chest Pain Weakness or transient paralysis of legs tachycardia ```
31
Chronic Venous Insufficiency (CVI)
is a condition that occurs when the vein wall and/or valves in the leg veins do not work effectively, which impairs the ability for blood to return to the heart from the legs, resulting in venous-stasis
32
Chronic Venous Insufficiency (CVI) may result from
Vein wall degeneration, post-thrombotic valvular damage, chronic venous obstruction, or dysfunction of the muscular pumps.
33
Edema defined as
a clinically apparent increase in the interstitial fluid volume
34
Edema causes
Due to Increase in capillary pressure usually results from an elevation of venous pressure caused by obstruction to venous and/or lymphatic drainage. Imbalance of the Startling Forces
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Pitting edema 1+
Barely detectable impression when finger is | presssed into skin.
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Pitting edema 2+
Slight indentation. | 15 seconds to rebound
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Pitting edema 3+
Deeper indentation. | 30 seconds to rebound.
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Pitting edema 4+
> 30 seconds to rebound.
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PT Implications for CVI
Exercise increases muscle pump for venous return and kidney function to clear fluid Short walks with occupations involving prolonged sitting, weight shift in standing
40
Ulcers
A persistent discontinuity in the integrity | of skin despite sufficient time for healing
41
3 types of ulcers
Arterial, Venous, Neuropathic.
42
Arterial ulcers
Dorsal or Distal location (toes) Sharp margins Painful Pallor, loss of hair, nail dystrophy
43
Venous ulcers
Malleolar location (usually Medial) Irregular margins Hemosiderin staining (browning) Varicose veins and pitting edema
44
Neuropathic ulcers
``` Plantar location Metatarsal heads (especially 2nd ), sole of foot, balls of toes “Punched Out” margins, usually correspond to pressure point Insensate, patient often diabetic with peripheral neuropathy ```
45
Patients with venous ulcers tend to have
CVI
46
Patients with arterial ulcers tend to have
PAD
47
Wells Score for DVT (Deep vein Thrombosis)
Score >2.0 — High probability Score 1.0 to 2.0 — Moderate Score <2.0 — Low
48
Pulmonary Embolism (PE)
Usually occurs in patients with previous venous thrombosis or at risk Can lead to cor pulmonale and eventually death
49
Pulmonary Embolism (PE) symptoms
Dyspnea, Sharp chest pain, pain with breathing, tachypnea, tachycardia hemoptysis
50
Wells Score for PE
Score >6.0 — High probability Score 2.0 to 6.0 — Moderate Score <2.0 — Low
51
Ischemia
Is a condition of imbalance between myocardial O2 supply and demand often caused by atherosclerosis of the coronary arteries.
52
Causes of Increased demand in ischemia
Exercise, Cold weather (increased vascular resistance), mental/emotional stress, spontaneous changes in HR and BP
53
Angina
``` Chest pain or discomfort caused due to cardiac ischemia Heaviness, tightness, pressure Discomfort gradually builds Gradually subsides Episode Lasts (1-15 minutes) ```
54
3 Major Types of angina
Stable Unstable Printzemental
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Stable angina
``` Discomfort gradually builds Occurs with exercise at a predictable and consistent intensity Gradually subsides with rest Typically Lasts (2-5 minutes) Rarely more than 5-10 mins Improve with nitroglycerin ```
56
Unstable angina
Recent or acceleration of angina threshold; New onset < 2 months Symptoms at rest > 15-20 minutes. Gradually worsens in a crescendo-like pattern May not respond to Nitro or Rest Often precursor to MI
57
Acute coronary syndrome (ACS)/Myocardial Infarction
Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery
58
Type 1 MI
ST elevation and spike in troponin. The release of enzymes is used to see if someone has MI because people can have ST depression and still be having MI
59
factors that increase likelihood of MI
does it have to do with exertion, does it spread to L arm and described as pressure
60
factors that decrease likelihood of MI
sharp pain, not associated with exertion, if I poke your chest and it hurts, it is probably not MI, positional changes like if they have Chest pain while laying down but gets better after getting up.