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Cardiovascular pt 2 Flashcards

1
Q

Atherosclerosis

A

thickening and hardening of vessel wall
-accumulation of lipid-filled macrophages and formation of plaque on vessel wall
-not a dx, a pathologic process
-inflammatory

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2
Q

atherosclerosis is the leading cause of____

A

coronary artery dx and cerebrovascular dx

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3
Q

Risk factors of atherosclerosis

A

-genetics
- male/ post-meno women
-inflammation from bacterial infection(chlamydia, periodontal dx)

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4
Q

Causes of atherosclerosis

A

anything tht causes endothelial injury:
-smoking
-hypertension
-high blood glucose (dm)
obesity
high LDL, low HDL

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5
Q

lipoproteins

A

fats packaged together with proteins, used to deliver cholesterol to cells

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6
Q

Pathogenesis of atherosclerosis

A

-damaged endothelial cells
-LDL infiltration –> oxidation
-immune response; macrophages engulf and t cells activate (release cytokines)
-further damage to vessel wall
-further activation of immune cells
fibrous cap forms- can remain stable or rupture

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7
Q

vicious cycle of inflammation and necrosis

A

-further damage to vessel wall
-further activation of immune cells

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8
Q

Endothelial dysfunction

A

-injured ECs become inflamed, cant make normal amts of anti-thrombotics and vasodilators (NO and PGI2)
-local mo release inflammatory cytokines (TNF-a, IFN-y, IL-1)
-damages cells + inflammation =oxidative stress

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9
Q

LDL infiltration

A

-LDLs from plasma infiltrate the vessel wall, and become oxidized by: oxidative stress, inflammation, activated mo
-oxidized LDLs are toxic to ECs:more damage, infiltration and mo
-Mo engluf ox-LDLs–>foam cell
-fatty streak
-T-cells activate mo
-SMCS begin proliferation

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10
Q

Fatty streaks

A

for some ppl:
-appear in the aorta (1st decade of life)
-in coronary arteries ( 2nd decade)
-in cerebral arteries (3th and 4th)

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11
Q

SMCs begin proliferation

A

-contractile –> epithelial phenotype
-make collagen, stiffen vessel wall
-also take up ox-LDLs

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12
Q

fatty streak –> lesion

A

-fatty streaks turn into lesions (plaques)
-fibrous plaque is stable
-complicated lesion is one where cap is ruptured

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13
Q

necrotic cells

A

dead, lipid-filled mo (foam cells) and SMCs

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14
Q

Factors contributing to plaque rupture

A

-shear forces
-enzyme degradation (remodeling)
-physical trauma

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15
Q

____of plaques determines what organ affected by vessel occlusion and ischemia

A

Location

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16
Q

Plaque in coronary arteries

A

Myocardial ischemia

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17
Q

Plaque in cerebral arteries

A

Stroke

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18
Q

Plaque in renal arteries

A

Reno-vascular hypertension

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19
Q

_____underlying cause of 50% of all deaths

A

Atherosclerosis

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20
Q

Atherosclerosis treatments-reducing risk factors

A

-smoking cessation
-reducing serum levels of LDL -> statins
-increasing HDL (can reverse pathogenesis)
-managing HTN and DM
-reducing body weight (obesity leads to low grade inflammation TNF-a and IL-6)

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21
Q

detecting pre-clinical lesions

A

-CAD- Coronary calcium scan
-PAD- Ankle-brachial index

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22
Q

If a lesion has ruptured or obstructed blood flow___

A

Primary goal is to restore blood flow before too much ischemic damage occurs

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23
Q

Atherosclerosis treatments under investigation

A

-gene editing
-antioxidants
Effective in animal models

24
Q

Three conditions form a pathophysiologic continuum

A

CAD-Coronary artery disease, Myocardial ischemia, and myocardial infract

25
The three diseases
-are caused by limiting the hearts supply of oxygenated blood by damaging endothelium, causing inflammation, formation of fibrotic plaque -are the progressive impairment in pumping ability in the heart
26
CAD, MI and Myocardial ischemia conventional, non-modifiable risk factors
-advanced age (lots of EC damage, poor repair) -males, post-menopausal females -fam hx (genetic factors, shared environmental exposures)
27
CAD, MI and Myocardial ischemia conventional modifiable risk factors
-dyslipidemia (abnormal concentrations of serum lipoproteins) -smoking -DM, insulin resistance -obesity -HTN -sedentary lifestyle -atherogenic diet
28
CAD, MI and Myocardial ischemia non-traditional risk factors
-increased serum markers for inflammation and thrombosis -hyperhomocysteinemia -adipokines -coronary artery calcification and carotid wall thickness-degree of structural change incr risk
29
hyperhomocysteinemia
- lack of enzyme that breaks down homocysteine, associated with pathogenic events of atherosclerosis
30
hs-CRP
(acute phase reactant made in the liver)—>plauque related inflammation
31
Adipokines
-hormones -leptin and adiponectin released by adipose cells -have pro-inflammatory effects
32
Myocardial ischemia
Supply of coronary blood cannot meet demand of myocardium for O2 and nutrients
33
Myocardial ischemia caused by:
-HTN, cocaine abuse, excessive/excertion, thyrotoxicosis -atherosclerotic plaques in coronary vessels
34
Role of atherosclerosis for myocardial ischemia
-plaques can grow in size -ruptures plaque causes thrombosis -occluding vessel lumen—> ischemia
35
Myocardium becomes ischemic within_______of coronary occlusion. If ischemia persists longer than _____infarction will occur
10 seconds , 20 mins
36
Myocardial infraction
Result of prolonged disruption in blood flow; myocytes dies
37
Myocardial infraction- cell injury effects
-oxygen deprived -anaerobic respiration -accumulation of H+ and lactic acid -damaged myocytes trigger release of Epi and NE—> further stress on heart -reperfusion injury (ROS damage) -loss of contractility
38
Myocardial infraction- cell death
-after 20 min of ischemia, irreversible hypoxic injury -necrosis of dead myocytes-intracellular molecules relapsed into blood and lymph -troponin-can be measured clinically
39
Myocardial infraction- heart remodeling
-damaged cells are degraded and removed -fibroblasts proliferate —. Scar tissue -scar tissue is strong but lack contractility f healthy myocardium
40
Function changes in heart
Level of impairment depends in severity of damages -decreases cardiac contractility -altered LV compliance -decr stoke volume and dejection fraction -SA or AV node malfunction
41
Ischemia/infarct manifestations
-chest pain (angina pectoris) -70-80% of ischemia episodes asymptomatic -shock-if primary coronary vessels occluded, assc with septum damage, rupture of chamber wall -nausea/vomitting- due to activation of vagus nerve -trachycardia-increase Epi and NE to maintain stroke volume
42
Infarct diagnosed by___
ECG and alteration in serum biomarkers (troponin)
43
Half of all infarcts are_____ by any symptoms
NOT preceded
44
Infarct treatment
Initial: supplemental O2, aspirin (antithrombotic) Long-term:lifestyle, manage/treat co-existing condition (ACE inhibitors, beta-blockers, statins) -thrombolytic/ antithrombotic
45
Cardiomyopathies
-group of conditions that affect wall of heart -tissue remodeling due to ischemia or hypertension (usually) -often leads to heart failure
46
Dilated cardiopathy
-chambers stretched out, heart is globe-shaped -ventricular dilation leads in increase in intracranial volume -increase in preload (affects SV and CO)
47
Dilated cardiomyopathy causes
Genetic Infectious Starvation Alcohol
48
Most common cause of sudden death in athletes
Hypertrophic cardiomyopathy
49
Hypertrophic cardiomyopathy
-characterized by thickening of heart walls -response to increased afterload -loss of compliance, cannot adequate fill with blood (affects SV, and CO)
50
Hypertrophic cardiomyopathy CAUSES
HTN Genetic
51
Myocardial remodeling , Body compensates by activating_____
Symph NS and RAAS. -Dysfunction decreases CO, MAP -Myocardial cells remodel to adapt to extra stress
52
Heart failure
Inability of the heart to generate adequate cardiac output
53
Cmon risk factors for heart failure are____and ______
Ischemia and hypertension
54
Other risk factors for heart failure
-age, obesity, renal failure, myocarditis, alcoholism, congenital heart dx, cardiomyopathies
55
Types of heart failure
-systolic-heart cannot generate enough force to pump blood -diastolic-heart cannot dilate enough to fill with blood -left-sided-left side of heart most common -right-sided: affecting right side of heart - can be causes by pulmonary dx
56
Heart failure manifestations
-dyspnea or excertion -increases venous pressure, lung edema -insufficient CO, blood begins “backing up” -tissue edema, lower extremities, increase in capillary hydrostatic pressure prevents reabsorption of fluid

Pathophys (11 decks)

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