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Pathophys > Cardiovascular pt 2 > Flashcards

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
Q

The three diseases

A

-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
Q

CAD, MI and Myocardial ischemia conventional, non-modifiable risk factors

A

-advanced age (lots of EC damage, poor repair)
-males, post-menopausal females
-fam hx (genetic factors, shared environmental exposures)

27
Q

CAD, MI and Myocardial ischemia conventional modifiable risk factors

A

-dyslipidemia (abnormal concentrations of serum lipoproteins)
-smoking
-DM, insulin resistance
-obesity
-HTN
-sedentary lifestyle
-atherogenic diet

28
Q

CAD, MI and Myocardial ischemia non-traditional risk factors

A

-increased serum markers for inflammation and thrombosis
-hyperhomocysteinemia
-adipokines
-coronary artery calcification and carotid wall thickness-degree of structural change incr risk

29
Q

hyperhomocysteinemia

A
  • lack of enzyme that breaks down homocysteine, associated with pathogenic events of atherosclerosis
30
Q

hs-CRP

A

(acute phase reactant made in the liver)—>plauque related inflammation

31
Q

Adipokines

A

-hormones -leptin and adiponectin released by adipose cells
-have pro-inflammatory effects

32
Q

Myocardial ischemia

A

Supply of coronary blood cannot meet demand of myocardium for O2 and nutrients

33
Q

Myocardial ischemia caused by:

A

-HTN, cocaine abuse, excessive/excertion, thyrotoxicosis
-atherosclerotic plaques in coronary vessels

34
Q

Role of atherosclerosis for myocardial ischemia

A

-plaques can grow in size
-ruptures plaque causes thrombosis
-occluding vessel lumen—> ischemia

35
Q

Myocardium becomes ischemic within_______of coronary occlusion. If ischemia persists longer than _____infarction will occur

A

10 seconds , 20 mins

36
Q

Myocardial infraction

A

Result of prolonged disruption in blood flow; myocytes dies

37
Q

Myocardial infraction- cell injury effects

A

-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
Q

Myocardial infraction- cell death

A

-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
Q

Myocardial infraction- heart remodeling

A

-damaged cells are degraded and removed
-fibroblasts proliferate —. Scar tissue
-scar tissue is strong but lack contractility f healthy myocardium

40
Q

Function changes in heart

A

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
Q

Ischemia/infarct manifestations

A

-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
Q

Infarct diagnosed by___

A

ECG and alteration in serum biomarkers (troponin)

43
Q

Half of all infarcts are_____ by any symptoms

A

NOT preceded

44
Q

Infarct treatment

A

Initial: supplemental O2, aspirin (antithrombotic)
Long-term:lifestyle, manage/treat co-existing condition (ACE inhibitors, beta-blockers, statins)
-thrombolytic/ antithrombotic

45
Q

Cardiomyopathies

A

-group of conditions that affect wall of heart
-tissue remodeling due to ischemia or hypertension (usually)
-often leads to heart failure

46
Q

Dilated cardiopathy

A

-chambers stretched out, heart is globe-shaped
-ventricular dilation leads in increase in intracranial volume
-increase in preload (affects SV and CO)

47
Q

Dilated cardiomyopathy causes

A

Genetic
Infectious
Starvation
Alcohol

48
Q

Most common cause of sudden death in athletes

A

Hypertrophic cardiomyopathy

49
Q

Hypertrophic cardiomyopathy

A

-characterized by thickening of heart walls
-response to increased afterload
-loss of compliance, cannot adequate fill with blood (affects SV, and CO)

50
Q

Hypertrophic cardiomyopathy CAUSES

A

HTN
Genetic

51
Q

Myocardial remodeling , Body compensates by activating_____

A

Symph NS and RAAS.
-Dysfunction decreases CO, MAP
-Myocardial cells remodel to adapt to extra stress

52
Q

Heart failure

A

Inability of the heart to generate adequate cardiac output

53
Q

Cmon risk factors for heart failure are____and ______

A

Ischemia and hypertension

54
Q

Other risk factors for heart failure

A

-age, obesity, renal failure, myocarditis, alcoholism, congenital heart dx, cardiomyopathies

55
Q

Types of heart failure

A

-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
Q

Heart failure manifestations

A

-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 (8 decks)

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