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5 cardiovascular Flashcards

1
Q

Arteriosclerosis definition

A

General term, hardening of arteries by any means including chronic disease or abnormal thickening & hardening of vessel walls

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2
Q

Atherosclerosis definition

A

Form of arteriosclerosis, specifically fibrofatty lesions in intimal lining of large and medium sized arteries

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3
Q

Atheroma

A

Thickening/hardening caused by soft intra-arterial fat and fibrin deposits

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4
Q

Non modifiable cardiovascular risks

A

Men over 45
Postmenopausal women
Family hx of CVD (death of males under 55 women under 65)

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5
Q

Modifiable risk factors for CAD

A 
HTN
Smoking
Dyslipidemia (low HDL high LDL)
Hypercholesterolemia
THE BEETIES
Being fat AF
Inflammation
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6
Q

Frequency of atherosclerosis areas affected

A 
ABD aorta and iliac
Coronary arteries
Thoracic aorta and lower ext
Internal carotids
Cerebral arteries
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7
Q

Order of injury

A 
Vessel endothelial injury
Migration of inflammatory cells
Formation of lesions by
-fatty streak
-then fibrous plaque (atheroma)
-lesion complications
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8
Q

Vessel injury

A

From smoking, htn, eleveated LDL, diabetes, turbulent blood, increased fibrinogen, autoimmunity

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9
Q

Migration of inflammatory cells

A

Monocytes (macrophages) adhere to damaged endothelial area and migrate between cells, then engulf LDL

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10
Q

Fatty streak lesion

A

A flat yellow discoloration created by foam cells, transformed by macrophages and filled with LDLs and cholesterol

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11
Q

Fibrous plaque

A

Lesion of advanced atherosclerosis
Consisting of lipid-laden hypertrophied smooth muscle cells surrounded by collagen, elastic fibers, and a mucoprotein matrix
Formation of scar tissue forms fibrous cap

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12
Q

Fibrous plaque formation part 2

A

Lesion is white and narrows lumen.
Core consists of debris from cell necrosis, caused by insufficient blood supply and acculmualtion of both intracellular and excracellular lipids

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13
Q

Fun cholesterol fact

A

1% decrease in serum cholesterol is associated with a 2% decrease in CHD

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14
Q

Methionine

A

With B6 and B12 produces homocysteine which inhibits the anticoagulant cascade. Abundant in animal proteins

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15
Q

Three types of lesions

A

Fatty streak
Fibrous atheromatous plaque
Complicated legion

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16
Q

Complicated lesions

A

Have thin fragile caps and possible a larger lipid core. High risk for hemorrhage and thrombosis from inflammation, injury, or turbulent blood flow

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17
Q

Most frequent organs effected from atherosclerosis

A

Heart, brain, kidneys, lower extremities, small intestine

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18
Q

How do atherosclerotic lesions produce their effect

A

Narrowing of the vessel and producing ischemia
Plaque rupture or hemorrhage causing sudden occlusion from a delicate lesion
Thrombosis and emboli

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19
Q

Large arteries are usually effected by atherosclerosis in what way

A

Thrombus formation and weakening of the vessel wall

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20
Q

Medium size arteries are usually effected by atherosclerosis in what way

A

Coronary and cerebral arteries. From ischemia and infarction due to occlusion

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21
Q

Cardiovascular manifestations of atherosclerosis

A 
Stable, unstable angina
MI, HF
HTN
Cardiac arrest
aortic aneurysms
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22
Q

Neurological manifestations of athersclerosis

A

CVA, TIA, weak carotid pulses and carotid bruits

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23
Q

Peripheral vascular manifestations of atherosclerosis

A 
Cyanosis
Claudication
Weak pulses
Bruits
Ulcers
Limb loss
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24
Q

Claudication

A

/Cramping pain caused by too little blood flow, often set off my exercise.

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25
Renal manifestations of atherosclerosis
Stenosis Decreased function HTN Failure
26
Vasculitis is
Any vein/artery/capillary with inflammation. Involves endothelial cells and smooth muscle
27
Clinical manifestations of vasculitis
Fever, myalgia (muscle pain), arthralgia (joint pain), malaise
28
Causes of vasculitis
Direct tissue injury, infection agents or immune processes or secondary due to things like lupus. Physical agents sunburn, toxins and trauma.
29
Physical coronary blood flow regulation
Openings for coronary arteries originate in the root of the aorta, just past the valve, and so aortic blood pressure is responsible for perfusing the coronary arteries (and the heart is responsible for creating aortic blood pressure) The coronary arteries are perfused during diastole
30
Neural coronary regulation
From the ANS | Medulla Oblongata innervation at T4-T5 to influence ino, chrono and dromotropy
31
Metabolic effects on coronary regulation
K+. LA (?) CO2, adenosine, NO
32
CAD definition
Any vascular disorder that narrows or occludes CA
33
CAD times
Ischemia 8-10 seconds reversible Injury 30 minutes and reversible Infarct is greater than 30 minutes, necrosis occurs, irreversible
34
What effects myocardial oxygen SUPPLY
Blood flow O2 volume within blood RBC volume and function Hb volume and function
35
Determinants of myocardial oxygen demand
Heart rate, contractility, wall tension and thickness
36
How does heart rate effect MVO2
Increased heart rate requires more oxygen, yet subendocardial coronary flow is reduced because of the decreased diastolic filling time
37
Wall tension formula
RadiusXIVP/thickness | So an increase in radius or a decrease in thickness will increase wall tension
38
Wall tension MVO2
Both increase preload and afterload increases MVO2
39
MVO2 contractility
Increased contractility increases rate of wall stress which increases MVO2
40
Pathology of UA/NSTEMI three phases
Development of unstable plaque that ruptures The acute ischemic event Long term risk of recurrent events
41
Inflammation ACS
Cytokines cause fibrous cap to become thinner and more vulnerable
42
Causes of acute ischemic event
Increased MVO2 from hypertension/tachycardia or most commonly decreased O2 supply from from platelet rich thrombi or vasospasm
43
Pain specific to UA (needs one of three)
Pain at rest (or minimal exertion) lasting 20 minutes Severe and frank pain, new onset within the last month More severe, prolonged, or frequent than previously experiences
44
ECG for UA NSTEMI
Normal, or depressed ST with T wave changes
45
Artery percentages in STEMI
30-40% RCA 40-50% LAD 15-20% LCA
46
Timing of damage in MI
Loss of contraction in 60 seconds Cell structure changes in minutes Both those reversible Ischemic injuries cease function in minutes and necrosis occurs 20-40 minutes Gross tissue changes aren't apparent for hours
47
Ventricular remodelling
Ventricles changing shape, size, thickness comprising early wall thinning, healing, hypertrophy, dilation. The ventricles get weak in spots, grow in others to compensate, can cause aneurysm or HF
48
Two groups of atherosclerotic lesions
Fixed or stable (often SA) | Unstable or vulnerable (UA, MI)
49
How plaque ruptures
Usually emotional or physical stress to increase sympathetic tone Diurnal - usually most often first hour after rising (increase sympathetic tone)
50
Thrombosis and vessel occlusion
Plaque ruptures, exposing lipid core which provide stimulus for platelet aggregation and thrombi formation. Smooth muscle and foam cells produce TF which starts clotting cascade
51
Platelets effects on ACS
Release ADP, thromboxane A2, thrombin initiates aggregation process. Glycoprotein on platelet membrane activated Fibrinogen binds to activated glycoprotein receptors
52
Poons ACS catagories
Plaque disruption and platelet aggregation in UA | Thrombus (with more fibrinogen and therefore red) in NSTEMI, STEMI
53
Cardiac specific biomarkers
Troponin T (Tnt) and I (Int - cardiac specific) CK-MB (creatine kinase myoglobin) Troponin TC and I rise 3-7 hours and can stay elevated for 7-10 days CK-MB rises 4-8 and hit normal in 2-3 days Myoglobin rises 1 hour and peaks at 4-8 (not cardiac specific)
54
ACS vs CIHD
ACS has unstable atherosclerotic plaque, which has been disrupted CIHD has stable atheroslecrotic plaque or vasospasm
55
ECG changes
1mm in two contiguous leads | Q waves are 25% r wave, 0.04 long. Diminished R wave height
56
Which area is the first often effected and why
Subendo, least blood supply (has tips of coronary arteries)
57
Biomarkers specificity to cardiac
Troponin I and T are absolute | CK-MB is Highly specific but not absolute
58
RCA occlusion
30%, Posterior Septum involved
59
LCA occlusion
20%, lateral involvement
60
LAD occlusion
Sudden death, causes anterior infarction
61
STEMI layers
``` Transmural means all levels involved, usually from complete occlusion Partial thickenss (sub endo, non-transmural) are genereally partial occlusions ```
62
ACS presentation
Crushing, constricting Substernal Radiates L arm, neck, jaw Prolonged pain not relieved by rest or nitro (need opiates) N/V sweating SOB, syncope Anxiety, weakness in ext, fatigue, tachy, restless, feeling of impending doom. Pale cool moist skin
63
Risk factors for atypical presentations
Old beeties woman with HF
64
Anigina pectoris
Most common sign 70-80% have it Pain from lactic acid or ischemic myocardium irritating the nerves Afferent nerves enter from C3-T4
65
Functional changes of MI
``` Decrease contractility (abnormal wall motion) Altered LV compliance Decrease SV Increased LVEDP SA malfunction Dysrhythmias HF ```
66
Factors for complications in MI
Patients pre-infarct condition | Size, location, extend of necrosis
67
Complications from MI
``` Dysrhythmias (90% from MI) LV failure Lower SV (causing cardiogenic shock) Pericarditis Heart rupture ```
68
Chronic ischemic heart disease
Characterize by SA, caused by stable atherosclerotic plaque or vasospasm, causing recurrent and transient episodes of ischemia - Stable angina - Variant Angina - Silent MI are all CIHD
69
Stable angina
From stable atherosclerotic plaque, increased MVO2 can't be met due to narrowing of lumen/stiffening of artery wall/lack of vessel dilation. Often a precursor to AMI
70
Pain differences in stable angina
Predictable causes Relieved by rest and nitrates Same type of pain from previous attacks
71
Variant angina
Prinzmetal or vasospastic. Coronary spasm from: Endothelial damage Hyperactive sympathetic nervous system Defects in interaction of calcium with vascular smooth muscle Nitric Oxide production deficits Impaired production of prostaglanding I2 (vasoconstrictor) or thromboxane A2 (role of inflammation)
72
More on variant angina
Exacerbations not related to MVO2 Has nocturnal instead of diurnal relationship Often associated with arrhythmias
73
Silent MI
Defined as objective evidence in absence of angina Objective evidence includes ST segment shifts Could be from low acuity or autonomic neuropath or increased pain thresholds

Pathology (24 decks)

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