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Pathophysiology > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

What are the valves on the R side of the heart?

A

Pulmonic valve, tricuspid

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2
Q

What are the valves on the L side of the heart?

A

Mitral, aortic valve

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3
Q

What are elastic arteries?

A

Thick tunica media with more elastic fibers (ex: aorta and pulmonary trunk), need to be able to stretch

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4
Q

What are muscular arteries?

A

Contain more muscle fibers than elastic arteries, main goal is to distribute blood to arterioles throughout body, vasoconstrict/dilate and control where blood goes

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5
Q

What is the role of natriuretic peptides?

A

Proteins that the heart releases in response to wall strain and tension, involved in sodium excretion,helps to vasodilate, can be measured to determine if HF is present

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6
Q

What are some of the consequences of hypertension?

A

Sustained elevation in pressure promotes vascular remodelling–results in tunica intima undergoing fibrosis and tunica media undergoing hypertrophy and hyperplasia

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7
Q

How is cholesterol transported in the body?

A

Via lipoproteins

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8
Q

What is the role of apolipoproteins?

A

Structural role, ligands for receptors, guide formation of lipoproteins, serve as activators or inhibitors of enzymes involved in metabolism of lipoproteins

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9
Q

What are lipoproteins composed of?

A

Phospholipids, cholesterol, protein, and triglycerides–composition varies

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10
Q

What are the four main lipoproteins?

A

Chylomicrons, VLDL, LDL, and HDL

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11
Q

What helps to break down lipoproteins?

A

Lipase (digestive enzyme released by pancreas)

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12
Q

What is the primary transportation system of cholesterol in the body?

A

LDL

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13
Q

Which lipoprotein takes cholesterol back to the liver?

A

HDL via reverse cholesterol transport

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14
Q

What is familial hypercholesterolemia?

A

Abnormal concentrations of serum lipoproteins due to genetic and dietary factors

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15
Q

What are some clinical manifestations of familial hypercholesterolemia?

A

Tendon xanthomas–cholesterol deposits in the tendons (often to dorsal surface of hands and Achilles tendon)

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16
Q

What is metabolic syndrome?

A

Compilation of conditions that increase person’s risk of diabetes and CVD

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17
Q

What is the diagnostic criteria for metabolic syndrome?

A

If have three of more of following: increased waist size, high fasting BG, high triglyceride levels, low HDL, and hypertension

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18
Q

What are the four steps in the progression of athleroscleosis?

A

Damaged endothelium, fatty streaks, fibrous plaque, and complicated plaque

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19
Q

What are foam cells?

A

Macrophages with undigested LDL

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20
Q

What is a fatty streak?

A

An early athlerosclerotic lesion–the accumulation of LDL, immune cells, and foam cells within vascular wall

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21
Q

What initiates damaged endothelium in athlerosclerosis?

A

Common risk factors contribute to damage

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22
Q

What is a complicated plaque in athlerosclerosis?

A

Ruptured atherosclerotic lesion that initiates the formation of a thrombus

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23
Q

When does a myocardial infarction occur?

A

With persistent ischemia or the complete occlusion of a coronary artery

24
Q

Which area of the heart does the L anterior descending coronary artery serve?

A

Left ventricle and L anterior side (front of L side)

25
Q

Which area of the heart does the circumflex artery serve?

A

Wraps around L side

26
Q

Which area of the heart does the R coronary artery serve?

A

R side and inferior wall

27
Q

Where are the myocardial nerve fibers located?

A

Along C3-T4

28
Q

When does unstable angina occur?

A

When superficial erosion of plaque leads to transient episodes of thrombotic vessel occlusion and vasoconstriction at site of plaque damage

29
Q

What is prinzmetal angina?

A

Uncommon, reduced blood flow to myocardium d/t coronary artery spasm, can occur to arteries that may or may NOT be affected by athlerosclerosis –occurs at rest and during sleep

30
Q

Why does N & V occur with MI?

A

Reflex stimulation of vomiting centers via pain fibers

31
Q

How long can cardiac cells withstand ischemia for?

A

20 min before irreversible cell death occurs

32
Q

What is troponin?

A

Protein, released from damaged cell membrane

33
Q

What can be released during ischemia?

A

Catecholamines (by myocardial cells), norepinephrine and angiotensin II

34
Q

What is hibernating myocardium?

A

Tissue that undergoes metabolic adaptation to prolong myocardial survival until perfusion restored

35
Q

What is ischemia reperfusion injury?

A

Results from generation of highly reactive oxygen intermediates (oxidative stress)–radicals cause further membrane damage and mitochondrial calcium overload

36
Q

What happens after MI?

A

Necrotic tissue at site of infarction replaced by fibrotic scar tissue within 24 hours

37
Q

How long does it take for the scar tissue to fully replace?

A

6 weeks post- MI, until then collagen matrix that is deposited is weak (mushy, vulnerable to injury)

38
Q

What is post- MI remodelling?

A

Myocyte hypertrophy, loss of contractile function in area of heart distant from infarction site, mediated by catecholamines, aldosterone, inflammatory cytokines–contributes to long-term dysfunction and HF

39
Q

What is an individuals ejection fraction?

A

% of blood pumped out with each beat

40
Q

What is HF with reduced ejection fraction?

A

Less than 40% EF, issue with contractility and not getting enough blood out, tries to increase preload but not sustainable (activation of RAAS d/t lack of blood to kidneys)

41
Q

What is HF with preserved ejection fraction?

A

Heart with EF >50%, stiff heart, ventricles cannot relax/fill and thus doesn’t get enough blood, blood becomes backed up into L atrium and to pulmonary circulation

42
Q

Why do those with HF experience orthopnea?

A

D/t increased venous return when laying down–increases preload and increases filling pressures

43
Q

What is paroxysmal nocturnal dyspnea?

A

Waking up gasping for air, generally represents pulmonary congestion and L sided HF

44
Q

What is R sided HF?

A

R side has trouble moving blood forward, will back up into the system and see elevated jugular pressure, congestion to liver and peripheral tissues, gut edema

45
Q

What is L sided HF?

A

L side not pumping well, see pulmonary congestion, dyspnea, orthopnea, cough, oliguria

46
Q

What are ACE inhibitors?

A

Prevent angiotensin converting enzyme from activating angiotensin II which vasoconstricts

47
Q

What is claudication?

A

Impairment in walking/exercise due to ischemia in the extremities during times of increased oxygen demand, r/t peripheral artery disease

48
Q

What is PAD?

A

Occlusions of small arteries and arterioles (specifically below the knee) cause most of the gangrenous changes of the lower extremities, occur in patchy areas of feet and toes. Lesions begin as ulcers, progress to gangrene or osteomyelitis

49
Q

What promotes DVT?

A

Venous stasis, venous intimal damage (r/t trauma, venipuncture, IV meds), and hypercoaguable state (smoking, live disease, oral contraceptives, etc.)

50
Q

How is DVT diagnosed?

A

Serum D-dimer concentration, lower extremity compression Doppler U/S (if D-dimer neg, can rule out but if +, must confirm with U/S b/c D-dimer not specific)

51
Q

What is the pacemaker of the heart?

A

SA node

52
Q

What are baroreceptors?

A

Mechanoreceptors allowing for relaying information derived from blood pressure within the ANS, regulates peripheral resistance and CO

53
Q

What electrolyte allows for the plateau seen in the action potential of contractile cardiac cells?

A

Calcium. Influx allows for the lengthening of the action potential, allows for ventricle to contract effectively

54
Q

What is preload?

A

Can also be called end-diastolic pressure, pressure in ventricle at end of diastole

55
Q

What is afterload?

A

Pressures in vessels that ventricle must pump against to eject blood

56
Q
A

Pathophysiology (12 decks)

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