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Pathology > 5 cardiovascular > Flashcards

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
Q

Renal manifestations of atherosclerosis

A

Stenosis
Decreased function
HTN
Failure

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26
Q

Vasculitis is

A

Any vein/artery/capillary with inflammation. Involves endothelial cells and smooth muscle

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27
Q

Clinical manifestations of vasculitis

A

Fever, myalgia (muscle pain), arthralgia (joint pain), malaise

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28
Q

Causes of vasculitis

A

Direct tissue injury, infection agents or immune processes or secondary due to things like lupus.
Physical agents sunburn, toxins and trauma.

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29
Q

Physical coronary blood flow regulation

A

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

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30
Q

Neural coronary regulation

A

From the ANS

Medulla Oblongata innervation at T4-T5 to influence ino, chrono and dromotropy

31
Q

Metabolic effects on coronary regulation

A

K+. LA (?) CO2, adenosine, NO

32
Q

CAD definition

A

Any vascular disorder that narrows or occludes CA

33
Q

CAD times

A

Ischemia 8-10 seconds reversible
Injury 30 minutes and reversible
Infarct is greater than 30 minutes, necrosis occurs, irreversible

34
Q

What effects myocardial oxygen SUPPLY

A

Blood flow
O2 volume within blood
RBC volume and function
Hb volume and function

35
Q

Determinants of myocardial oxygen demand

A

Heart rate, contractility, wall tension and thickness

36
Q

How does heart rate effect MVO2

A

Increased heart rate requires more oxygen, yet subendocardial coronary flow is reduced because of the decreased diastolic filling time

37
Q

Wall tension formula

A

RadiusXIVP/thickness

So an increase in radius or a decrease in thickness will increase wall tension

38
Q

Wall tension MVO2

A

Both increase preload and afterload increases MVO2

39
Q

MVO2 contractility

A

Increased contractility increases rate of wall stress which increases MVO2

40
Q

Pathology of UA/NSTEMI three phases

A

Development of unstable plaque that ruptures
The acute ischemic event
Long term risk of recurrent events

41
Q

Inflammation ACS

A

Cytokines cause fibrous cap to become thinner and more vulnerable

42
Q

Causes of acute ischemic event

A

Increased MVO2 from hypertension/tachycardia or most commonly decreased O2 supply from from platelet rich thrombi or vasospasm

43
Q

Pain specific to UA (needs one of three)

A

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
Q

ECG for UA NSTEMI

A

Normal, or depressed ST with T wave changes

45
Q

Artery percentages in STEMI

A

30-40% RCA
40-50% LAD
15-20% LCA

46
Q

Timing of damage in MI

A

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
Q

Ventricular remodelling

A

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
Q

Two groups of atherosclerotic lesions

A

Fixed or stable (often SA)

Unstable or vulnerable (UA, MI)

49
Q

How plaque ruptures

A

Usually emotional or physical stress to increase sympathetic tone
Diurnal - usually most often first hour after rising (increase sympathetic tone)

50
Q

Thrombosis and vessel occlusion

A

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
Q

Platelets effects on ACS

A

Release ADP, thromboxane A2, thrombin initiates aggregation process.
Glycoprotein on platelet membrane activated
Fibrinogen binds to activated glycoprotein receptors

52
Q

Poons ACS catagories

A

Plaque disruption and platelet aggregation in UA

Thrombus (with more fibrinogen and therefore red) in NSTEMI, STEMI

53
Q

Cardiac specific biomarkers

A

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
Q

ACS vs CIHD

A

ACS has unstable atherosclerotic plaque, which has been disrupted
CIHD has stable atheroslecrotic plaque or vasospasm

55
Q

ECG changes

A

1mm in two contiguous leads

Q waves are 25% r wave, 0.04 long. Diminished R wave height

56
Q

Which area is the first often effected and why

A

Subendo, least blood supply (has tips of coronary arteries)

57
Q

Biomarkers specificity to cardiac

A

Troponin I and T are absolute

CK-MB is Highly specific but not absolute

58
Q

RCA occlusion

A

30%, Posterior Septum involved

59
Q

LCA occlusion

A

20%, lateral involvement

60
Q

LAD occlusion

A

Sudden death, causes anterior infarction

61
Q

STEMI layers

A 
Transmural means all levels involved, usually from complete occlusion
Partial thickenss (sub endo, non-transmural) are genereally partial occlusions
62
Q

ACS presentation

A

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
Q

Risk factors for atypical presentations

A

Old beeties woman with HF

64
Q

Anigina pectoris

A

Most common sign 70-80% have it
Pain from lactic acid or ischemic myocardium irritating the nerves
Afferent nerves enter from C3-T4

65
Q

Functional changes of MI

A 
Decrease contractility (abnormal wall motion)
Altered LV compliance 
Decrease SV
Increased LVEDP
SA malfunction
Dysrhythmias 
HF
66
Q

Factors for complications in MI

A

Patients pre-infarct condition

Size, location, extend of necrosis

67
Q

Complications from MI

A 
Dysrhythmias (90% from MI) 
LV failure
Lower SV (causing cardiogenic shock)
Pericarditis 
Heart rupture
68
Q

Chronic ischemic heart disease

A

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
Q

Stable angina

A

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
Q

Pain differences in stable angina

A

Predictable causes
Relieved by rest and nitrates
Same type of pain from previous attacks

71
Q

Variant angina

A

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
Q

More on variant angina

A

Exacerbations not related to MVO2
Has nocturnal instead of diurnal relationship
Often associated with arrhythmias

73
Q

Silent MI

A

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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