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Cardiopulmonary > Cardiovascular disease and atherosclerosis > Flashcards

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
Q

Risk Factors aneurysms

A 
Cardiovascular disease and Risk factors for CVD
Especially smoking
Male
Genetics (Marfan’s)
40-60 yr old
Hypertension prevalent
26
Q

Types of Aneurysms

A

Saccular aka Berry
Fusiform
Dissecting

27
Q

Saccular aka Berry Aneurysms

A

Small, spherical, 1-1.5 cm.

Most common in brain tissue

28
Q

Fusiform Aneurysms

A

Gradual more progressive

29
Q

Dissecting Aneurysms

A

Blood filled channel within vessel wall

30
Q

Abdominal Aortic Aneurysm symptoms

A 
Dull, tearing ache/pain in low back,
groin or mid abdominal left flank
Chest Pain
Weakness or transient paralysis of legs
tachycardia
31
Q

Chronic Venous Insufficiency (CVI)

A

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
Q

Chronic Venous Insufficiency (CVI) may result from

A

Vein wall degeneration, post-thrombotic valvular damage, chronic venous obstruction, or dysfunction of the muscular pumps.

33
Q

Edema defined as

A

a clinically apparent increase in the interstitial fluid volume

34
Q

Edema causes

A

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

35
Q

Pitting edema 1+

A

Barely detectable impression when finger is

presssed into skin.

36
Q

Pitting edema 2+

A

Slight indentation.

15 seconds to rebound

37
Q

Pitting edema 3+

A

Deeper indentation.

30 seconds to rebound.

38
Q

Pitting edema 4+

A

> 30 seconds to rebound.

39
Q

PT Implications for CVI

A

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
Q

Ulcers

A

A persistent discontinuity in the integrity

of skin despite sufficient time for healing

41
Q

3 types of ulcers

A

Arterial, Venous, Neuropathic.

42
Q

Arterial ulcers

A

Dorsal or Distal location (toes)
Sharp margins
Painful
Pallor, loss of hair, nail dystrophy

43
Q

Venous ulcers

A

Malleolar location (usually Medial)
Irregular margins
Hemosiderin staining (browning)
Varicose veins and pitting edema

44
Q

Neuropathic ulcers

A 
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
Q

Patients with venous ulcers tend to have

A

CVI

46
Q

Patients with arterial ulcers tend to have

A

PAD

47
Q

Wells Score for DVT (Deep vein Thrombosis)

A

Score >2.0 — High probability
Score 1.0 to 2.0 — Moderate
Score <2.0 — Low

48
Q

Pulmonary Embolism (PE)

A

Usually occurs in patients with previous venous thrombosis or at risk
Can lead to cor pulmonale and eventually death

49
Q

Pulmonary Embolism (PE) symptoms

A

Dyspnea, Sharp chest pain, pain with breathing, tachypnea, tachycardia hemoptysis

50
Q

Wells Score for PE

A

Score >6.0 — High probability
Score 2.0 to 6.0 — Moderate
Score <2.0 — Low

51
Q

Ischemia

A

Is a condition of imbalance between myocardial O2 supply and demand often
caused by atherosclerosis of the coronary arteries.

52
Q

Causes of Increased demand in ischemia

A

Exercise, Cold weather (increased vascular resistance), mental/emotional stress, spontaneous
changes in HR and BP

53
Q

Angina

A 
Chest pain or discomfort  caused due to cardiac ischemia
Heaviness, tightness, pressure
Discomfort gradually builds
Gradually subsides
Episode Lasts (1-15 minutes)
54
Q

3 Major Types of angina

A

Stable
Unstable
Printzemental

55
Q

Stable angina

A 
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
Q

Unstable angina

A

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
Q

Acute coronary syndrome (ACS)/Myocardial Infarction

A

Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery

58
Q

Type 1 MI

A

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
Q

factors that increase likelihood of MI

A

does it have to do with exertion, does it spread to L arm and described as pressure

60
Q

factors that decrease likelihood of MI

A

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.

Cardiopulmonary (7 decks)

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