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Pathophysiology exam 2 > CV disorders > Flashcards

CV disorders Flashcards

1
Q

What is ischemia?

A

Reduction in blood flow that doesn’t meet needs for oxygen

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2
Q

What is infarction?

A

Necrotic tissue resulting from prolonged ischemia

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3
Q

What is the leading cause of death in the US?

A

Atherosclerosis

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4
Q

Why do men have a higher risk for atherosclerosis?

A

Estrogen has protective factors against cardiac disease

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5
Q

How does cholesterol get where it needs to go in the body?

A

Lipoproteins; they carry a core of cholesterol

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6
Q

What do LDLs do?

A

Deposit cholesterol in distal tissues -> atherosclerosis

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7
Q

What do HDLs do?

A

They are cardioprotective - they take cholesterol from distal portions and bring it to the liver to metabolize

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8
Q

How is HTN a risk factor for atherosclerosis?

A

HTN can cause microtears in the blood vessels

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9
Q

How is DM a risk factor for atherosclerosis?

A

Glycation end products (products of glucose metabolism) can rise too much and cause microtears in blood vessels
Can allow entry of lipids into blood vessels

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10
Q

What are the 3 types of lesions in atherosclerosis?

A

Fatty streak
Fibrous atheromatous plaque
Complicated lesion

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11
Q

What is a fatty streak?

A

Early discoloration of the intima due to infiltration by macrophages and lipids

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12
Q

What is a fibrous atheromatous plaque?

A

Further invasion of the intima, triggering the inflammatory process

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13
Q

What is a complicated lesion?

A

Hemorrhage within the lesion or ulceration of the lesion, leading to thrombosis

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14
Q

What happens in a fatty streak?

A

Development begins under the blood vessel -> influx of monocytes -> monocytes become macrophages -> macrophages eat all the lipids -> development of fatty streak

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15
Q

How does a fatty streak turn into a fibrous atheromatous plaque?

A

The inflammatory process is initiated

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16
Q

What happens in a fibrous atheromatous plaque?

A

The vessel becomes less elastic

Subendothelial is exposed to material in the blood stream -> clotting

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17
Q

What is the process of atherosclerosis?

A

Endothelial injury -> fatty streak -> smooth muscle tries to repair damage -> fibrous atheromatous plaque -> complicated lesion

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18
Q

What is the process of atherosclerosis? (with details of each step)

A

Endothelial injury occurs and allows the entry of lipids into intima
Fatty streak develops
- Monocytes migrate into vessel wall
- Monocytes differentiate into macrophages
- Release toxic oxygen to oxidize LDL
- Toxic oxygen further damages endothelium
- Platelets adhere to damages endothelium
- Monocytes engulf lipids and become “foam cells”
Smooth muscle tries to repair damage
- Foam cells recruit smooth muscle cells
- Smooth muscle proliferates and produces ECM (collagen)
Fibrous atheromatous plaque forms
- Superficial smooth muscle cap is created
- Macrophages, lymphocytes, foam cells, smooth muscle cells, fatty debris are under fibrous cap
- Core can be necrotic and unstable
- Can extend into lumen, slowing blood flow
Complicated lesion
- Unstable cap can rupture (or keep growing and occlude vessel
- Coagulation cascade initiated

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19
Q

What is stable angina?

A

Chest pain occurring from the demand of oxygen outweighing the supply of oxygen

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20
Q

How does pain in stable angina occur?

A

Prolonged ischemia -> anaerobic metabolism (instead of aerobic) -> build up of lactic acid

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21
Q

What is coronary blood flow regulated by?

A

Cardiac oxygen

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22
Q

What are oxygen requirements dependent on?

A

Metabolic activity of the heart

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23
Q

What are the two types of plaques in ACS?

A

Stable plaque and unstable plaque

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24
Q

What is a stable plaque?

A

A plaque that obstructs blood flow over time

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25
Q

What is an unstable plaque?

A

Plaque (with a rigid cap) that can rupture due to hemodynamic stress -> expose lipid core to blood -> stimulate platelet aggregation/thrombus formation -> smooth muscle/foam cells stimulate extrinsic pathway -> result in acute vascular occlusion

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26
Q

In ACS, what is the extent of damage dependent on?

A

Location of occlusion
Extent and duration of occlusion
Amount of tissue supplied by the vessel
Metabolic needs of the heart

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27
Q

How can ischemia affect the 3 layers of the heart?

A

All layers can be affected (transmural) or only some

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28
Q

Which area of the heart is affected first in ischemia?

A

The area below the endocardium

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29
Q

What areas of the heart will a right coronary artery obstruction affect?

A

Right atrium/right ventricle

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30
Q

What areas of the heart will a left main coronary artery obstruction affect?

A

Septum, anterior wall of left ventricle, lateral wall of left ventricle, posterior wall

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31
Q

What is a left main coronary artery obstruction called and why?

A

Widow maker because it obstructs blood flow to the circumflex and left anterior descending arteries

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32
Q

Why is the area below the endocardium affected first during an MI?

A

Coronary arteries run outside epicardium and send in feeding blood vessels that penetrate
Arteries have highest % of blood oxygen -> when it penetrates down, the tissue around will extract O2 -> decrease in O2 as you go deeper from epicardium to endocardium

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33
Q

How long do you have to reverse damage from ACS?

A

About 40 minutes

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34
Q

What happens in ACS?

A

Damage from anaerobic metabolism
- No energy
- Decrease in contractile force
- Glycogen depletion and mitochondrial swelling
- Failure of LV to pump possible
Ventricular remodeling to compensate for infarcted areas (which become thin and dilated)

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35
Q

How is stable angina presented?

A

Pain associated with exertion and relieved by rest
Constricting, squeezing, stabbing
Consistent with same intensity and character

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36
Q

How is stable angina pain relieved?

A

Rest or nitroglycerin

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37
Q

How can you get acute coronary syndrome?

A

May result from stable angina or without warning

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38
Q

What is unstable angina/NSTEMI and what are characteristics?

A

Pain at rest
Pain may vary in intensity, frequency, character
Differentiate based on biomarkers

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39
Q

What is STEMI and what are characteristics?

A

Myocardial infarction
Could be acute onset or progression from NSTEMI
Crushing, suffocating, constricting substernal pain
Prolonged pain
Radiates to jaw, neck, left arm
Nausea and vomiting
Fatigue and weakness

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40
Q

What are biomarkers of USA?

A

Creatine kinase myocardial band
Troponin (elevation is more specific to cardiac tissue -> damage has been done to cardiac tissue -> more helpful in diagnosis)

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41
Q

How do you interpret EKG in the context of MI?

A

ST depression -> ischemia (recoverable - can restore blood flow)
ST elevation -> sign of myocardial injury (cannot recover after this)

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42
Q

What is heart failure?

A

Disorder where the heart is unable to pump a sufficient amount of blood to meet the body’s demands

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43
Q

What is preload?

A

Volume of blood that stretches the ventricle at the end of diastole

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44
Q

What is afterload?

A

Force the ventricle has to overcome to get the blood out

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45
Q

What is contractility?

A

The contractile force of the ventricle - how well does the heart contract?

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46
Q

Why is having too much preload bad?

A

Having too much blood stretches the heart muscle and can cause the actin and myosin fibers to no longer be touching, so the ventricle can’t contract well (dilated cardiomyopathy)

47
Q

What is systolic dysfunction in HF?

A

Decrease in cardiac contractility

EF <50%

48
Q

What happens in systolic dysfunction in HF?

A

Preload increases -> ventricle dilates -> increased left ventricular end diastolic pressure -> pulmonary HTN -> pulmonary edema

49
Q

What is the etiology of systolic dysfunction?

A

Impaired contractility
Volume overload
Pressure overload

50
Q

What can cause systolic dysfunction?

A

LV dilation to accommodate pressure increase in right side of the heart -> increased preload -> volume increase
Ischemic heart disease -> can’t get blood out -> EF drops
Cardiomyopathy (heart becomes rigid) -> weak contraction
Volume overload - floppy valve somewhere
Pressure overload - high pressure in aorta -> afterload increase -> ventricle squeezes and meets resistance to get blood out

51
Q

What is diastolic dysfunction in HF?

A

Abnormal relaxation of ventricles

52
Q

In what populations is diastolic dysfunction higher?

A

Women, obesity, HTN, DM

53
Q

What is the etiology of diastolic dysfunction?

A

Impaired ability of ventricle to expand
Increased wall thickness and reduced LV chamber size
Delayed diastolic relaxation - ventricle begins to fill while still stiff

54
Q

What is a good metaphor to remember diastolic dysfunction by?

A

Filling up a stiff balloon with air - have to overcome the initial stiffness to get air in

55
Q

How does diastolic dysfunction affect the heart pumping blood?

A

Normal ejection fraction, but start with a low volume

56
Q

What can cause diastolic dysfunction in HF?

A

Pericardium issues (ex: fluid accumulation, leading to restriction)

57
Q

What is delayed diastolic relaxation?

A

Phase in diastole where it actively relaxes and pulls blood down from the atrium

58
Q

What are symptoms of right ventricular dysfunction in HF?

A

Systemic symptoms

Peripheral edema, liver congestion, anorexia, elevated JFC

59
Q

What are symptoms of left ventricular dysfunction in HF?

A

Initially pulmonary and progress to systemic

Activity intolerance, cyanosis, hypoxia, orthopnea, paroxysmal nocturnal dypsnea

60
Q

What happens in left ventricular dysfunction?

A

Blood won’t make it to the rest of the body
No O2 to peripheral tissues/brain
Fatigue/lightheadedness
Pressure build up to capillaries in lungs -> fluid in lungs

61
Q

What happens in right ventricular dysfunction?

A

Less volume to the lungs
Built up pressure into the system - RA -> vena cava -> jugular veins -> liver -> fluid leaking out of capillaries -> liver congestion/edema

62
Q

What is an aneurysm?

A

An abnormal localized dilation of blood vessel

63
Q

What is the etiology of aneurysms

A

Weakness in blood vessel caused by congenital defect, trauma, infection, atherosclerosis
Aneurysm growth can put pressure on surrounding structures or rupture

64
Q

How do aneurysms manifest?

A

Depends on location
Some possibilities:
- Asymptomatic
- Substernal, back, neck pain
- Dyspnea and cough if tracheal impingement
- Hoarseness if pressure on laryngeal nerve
- Difficulty swallowing if pressure on esophagus

65
Q

What is an aortic dissection?

A

Hemorrhage into vessel wall that tears along the length of the vessel
- Can coagulate and obstruct other vessels

66
Q

What vessel is more affected in aortic dissections?

A

Ascending aorta

67
Q

What is the etiology of an aortic dissection?

A

Weakness of vessel, HTN, connective tissue diseases, surgery increasing risk

68
Q

What is the epidemiology of aortic dissections?

A

Most common in men between 40 and 60

69
Q

How do aortic dissections manifest?

A

Abrupt, excruciating tearing or ripping pain
BP and pulse unobtainable in area
Syncope, paralysis, hemiplegia could occur

70
Q

What can happen in an aortic dissection of the common carotid?

A

Obstruction of brain - complaints of lightheadedness

71
Q

What can happen in an aortic dissection of the left subclavian?

A

Issues with left arm

72
Q

What can happen in an aortic dissection of the ascending aorta?

A

Can obstruct vessels that branch off

73
Q

What is hypertrophic cardiomyopathy?

A

Unexplained LV hypertrophy

74
Q

With what is hypertrophic cardiomyopathy associated?

A

Thickened ventricular septum, abnormal filling during diastole, LV outflow obstruction
- Most common cause of sudden death in athletes

75
Q

What is the etiology of hypertrophic cardiomyopathy?

A

Autosomal dominant genetic predisposition

Abnormal coding for cardiac muscle proteins

76
Q

What is pericarditis?

A

Inflammation of pericardium

Stiff pericardium makes it difficult for the heart to expand

77
Q

What is the etiology of pericarditis?

A

Infection, trauma, medications

78
Q

What does pericarditis often lead to?

A

Pericardial effusion -> increased fluid volume in pericardial sac -> increased pressure on heart

79
Q

How does pericarditis affect pressure around the heart?

A

Pressure on right side are lower and more vulnerable to being compressed, so manifestations typically appear as right sided heart failure
Decreased venous return -> decreased preload -> tachycardia to compensate

80
Q

How does pericarditis affect the right side of the heart?

A

Right chambers are squeezed -> symptoms of right sided heart failure
Pressure built in RV -> RV won’t take blood from RA -> high afterload in RA -> low volume of blood making it to the body -> BP goes down -> stretch receptors in aorta sense low volume -> sensors compensate by increased HR

81
Q

What is endocarditis?

A

Infection of the heart lining

82
Q

What is the etiology of endocarditis?

A

Invasion of heart valves and endocardium by bacteria -> bacteria into blood stream -> endothelial damage, altered hemodynamics, bacteremia lead to thrombus -> thrombus seeded by bacteria -> development/growth of friable vegetations -> destruction of cardiac tissue

83
Q

What are vegetations?

A

Calcium based deposits that develop on valves as a result of bacteria initiating damage

84
Q

Which valves are most commonly affect in endocarditis?

A

Aortic and mitral

85
Q

How does endocarditis manifest?

A

Fever, murmur, splinter hemorrhages

86
Q

What are splinter hemorrhages?

A

Tiny vegetations crack off and travel and obstruct tiny vessels

87
Q

How is mitral valve prolapse related to endocarditis?

A

The mitral valve balloons back up into the atrium and increases the risk of development

88
Q

What is rheumatic heart disease?

A

When a deformity of heart valves occurs

89
Q

How does one get rheumatic heart disease?

A

The body creates an autoimmune response against the M protein on group A beta-hemolytic strep
Antibodies are created and react with antigens in the body
Antibodies bind to receptors on heart valve -> vegetations -> Aschoff bodies develop -> valves become stenotic

90
Q

What are aschoff bodies?

A

Necrotic tissue surrounded by immune cells

91
Q

How does rheumatic heart disease manifest?

A

Arthralgia to severe arthritis
Vegetations and scarring causing deformities
Subcutaneous nodules over extensor muscles of wrist, elbow, ankle, knee

92
Q

Which valves are most commonly affected in rheumatic heart disease?

A

Mitral/aortic

93
Q

What is the difference between rheumatic heart disease and endocarditis?

A

RHD is abnormal response to M protein

Endocarditis is bacterial introduction to the body

94
Q

What are the 5 types of valvular heart disease?

A 
Mitral valve stenosis
Mitral valve regurgitation
Mitral valve prolapse
Aortic stenosis
Aortic regurgitation
95
Q

What happens in mitral valve stenosis?

A

Narrow mitral valve from rheumatic fever or congenital abnormality
Fibrous replacement of valve resulting in stiff valves
Increased resistance -> pulmonary vascular congestion

96
Q

What happens in mitral valve regurgitation?

A

Valve doesn’t close properly from rheumatic heart disease, rupture chordae tendinae, ruptured papillary muscles, LV dilation
Bidirectional flow -> increased pressure in RA -> chamber dilation -> pulmonary congestion

97
Q

What happens in MVP?

A

“Floppy” valve from genetic disorder -> fibrotic changes develop on valves - can cause mitral regurgitation
Valve “balloons” up into LA -> some regurgitation -> bidirectional flow -> dilation in LA -> pulmonary congestion

98
Q

What happens in aortic stenosis?

A

Narrow aortic valve lumen - congenital or calcification

Impaired LV outflow -> LV hypertrophy to accommodate -> increase cardiac workload -> angina, syncope, heart failure

99
Q

What happens in aortic regurgitation?

A

Incompetent atrial valve allows backflow from aorta to LV - rheumatic fever, congenital abnormalities, aortic dilation
Ventricle squeezes -> bidirectional flow -> residual blood in LV -> pressure increases -> chamber size decreases

100
Q

What is congenital heart disease?

A

Birth defect occurring in the heart between 4th and 7th week of gestation - genetic and environmental influences

101
Q

What happens in congenital heart disease?

A

Shunting of blood to path of least resistance
Cyanosis
Disruption of pulmonary blood flow

102
Q

What is the difference between left to right shunt and right to left shunt in congenital heart disease?

A

LTR are usually acyanotic
- Patent ductus arteriosus, septal defects
RTL shunts are usually cyanotic
- Tetralogy of Fallot, transposition of great vessels

103
Q

What happens during the disruption of pulmonary blood flow?

A

Reduced pulmonary blood flow causes fatigue, dyspnea
- Pulmonary stenosis
Increase in pulmonary blood flow stimulates vasoconstriction of pulmonary artery
Pulmonary HTN can occur in LTR shunts
Pulmonary stenosis + hole will force blood to the left side of the heart

104
Q

What is patent ductus arteriosus?

A

Channel that goes from pulmonary artery to aorta in utero

105
Q

What happens in congenital patent ductus arteriosus?

A

Hole stays open, so blood with go from aorta -> pulmonary artery -> lungs -> LA -> LV -> some oxygenated blood to aorta and some oxygenated blood out of pulmonary artery (cyanotic)

106
Q

What is patent foramen ovale?

A

Congenital heart disease

Persistent opening in atrial or ventricular septum

107
Q

What happens in patent foramen ovale (atrial septum)?

A

Can develop L to R shunt
Dilation of R heart
Fixed split S2 due to delayed closure of pulmonic valve
Oxygenated blood -> LV -> L to R because of pressure difference

108
Q

What are the types of patent foramen ovale?

A

Congenital abnormalities in atrial/ventricular septum

109
Q

What happens in patent foramen ovale (ventricular septum)?

A

Can be asymptomatic or can develop heart failure
Can develop L to R shunt
Tachypnea, diaphoresis, failure to thrive
Pulmonary HTN due to increased volume
Can develop increase in pulmonary vascular resistance
Cyanosis from no O2 making it to the body

110
Q

What are the 4 defects of Tetralogy of Fallot?

A

Ventricular septal defect
Shifting of aorta to the right
Pulmonary outflow obstruction
Right ventricular hypertrophy

111
Q

What happens in Tetralogy of Fallot?

A

Deoxygenated blood sent through systemic circulation
Blood comes in RA -> RV (deoxygenated blood) -> tries to push out through pulmonary artery, but it’s stenotic -> goes through hole in septum -> blood leaves through to aorta and the rest of the body -> deoxygenated blood to the rest of the body -> cyanosis

112
Q

What is transposition of great vessels?

A

When the aorta rises from right ventricle, pulmonary artery arises from left ventricle

113
Q

What happens in transposition of great vessels?

A

Aorta and pulmonary artery are reversed
- RA -> RV -> aorta -> body (no oxygenation)
- LA -> LV -> pulmonary -> lungs (oxygenated blood never gets anywhere)
Ventricular septal defect present in 50%, allowing blood mixing
Cyanosis

Pathophysiology exam 2 (2 decks)

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