Blood Vessels and Cardiovascular System Pathology Flashcards
(108 cards)
1
Q
Cardiovascular System
(3)
A
*Blood vessels
*Heart
*(Blood)
2
Q
Mechanism of Vascular Disease
(3)
A
- Narrowing of lumen
- Obstruction of lumen
- Weakening of wall
3
Q
- Narrowing of lumen
(1)
A
–Athersclerosis
4
Q
- Obstruction of lumen
(2)
A
–Thrombus
–Embolus
5
Q
- Weakening of wall
(2)
A
–Dilation
–Rupture
6
Q
Arteriosclerosis
* Three patterns of arteriosclerosis
(3)
A
–Atherosclerosis
* Atheromas
–Arteriolosclerosis
–Medial Calcific Sclerosis
7
Q
Constitutional risk
factors (non-modifiable)
(4)
A
– Age
– Gender
– Family history
– Genetic abnormalities
8
Q
Major risk factors (modifiable)
(4)
A
– Hyperlipidemia
– Hypertension
– Cigarette smoking
– Diabetes mellitus
9
Q
Serum Lipids –Major Risk Factor
(3)
A
- Total Cholesterol (< 200 mg/dl)
- Low Density Lipoprotein (< 100 mg/dl)
- High Density Lipoprotein (> 40 mg/dl)
10
Q
- Low Density Lipoprotein (< 100 mg/dl)
(2)
A
– “Bad cholesterol”
– Delivers cholesterol to peripheral tissues
11
Q
- High Density Lipoprotein (> 40 mg/dl)
(2)
A
– “Good cholesterol”
– Mobilizes cholesterol from atheromas and transports it to the liver for excretion
12
Q
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Risk Factors for Atherosclerosis
* Additional risk factors
(8)
A
– Obesity
– Physical activity
– Personality type
– Alcohol
– Trans fatty acids
– Lipoprotein a
– Hyperhomocystinemia
– Systemic inflammatory state (C-reactive protein CRP)
13
Q
Atherosclerosis
A
- Atheromatous plaques project into and
obstruct the lumen and weaken the media
14
Q
Pathogenesis of Atherosclerosis
(2)
A
- A chronic inflammatory response of the arterial
wall initiated by injury to the endothelium - Atheromatous plaques located in intima
obstruct vessel lumen and weaken vascular wall
15
Q
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Pathogenic Events of
Atherosclerosis
(7)
A
- Endothelial Injury
- Accumulation of lipoproteins
- Monocyte adhesion to the endothelium
- Platelet adhesion
- Factor release from activated platelets,
macrophages, endothelial cells - Smooth muscle cell proliferation and ECM
production - Lipid accumulation
16
Q
Progression of Atherosclerosis
(4)
A
- Fatty streak
- Atheroma (plaque) –
covered by fibrous cap - Complicated plaque –
ulcerated - Eventually clinical
events occur and
symptoms produced
17
Q
Fatty Streak
(2)
A
- Earliest lesion of atherosclerosis
- Lipid filled foam cells within the intima
18
Q
Atheroma
A
- Plague like lesion that begins in the intima
and impinges on lumen
19
Q
Complicated Plaque
A
- Ulceration exposes thrombogenic material
20
Q
Complications of Atheromas
(6)
A
- Ischemic injury - compromised blood flow to distal organs
- Disruption –exposes thrombogenic substances
- Thrombosis - clotting on surface of ulcerated plaque causes
further narrowing - Embolization –thrombus or plaque material may embolize
(thromboembolus) - Hemorrhage –a hematoma may expand or rupture plaque
- Aneurysm - weak wall may dilate and rupture
21
Q
Major Clinical Consequences of
Atherosclerosis
(4)
A
- Myocardial infarct -
heart attack - Cerebral infarct - stroke
- Aortic aneurysm -
rupture - Peripheral vascular
disease - gangrene of
legs
22
Q
Atherosclerosis
A
- Atheromatous plaques project into and
obstruct the lumen and weaken the media
23
Q
Arteriolosclerosis
(4)
A
- Hypertension
- Small blood vessel disease
- Hyaline Arteriolosclerosis
- Hyperplastic Arteriolosclerosis
24
Q
- Hyaline Arteriolosclerosis
A
–Diabetic microangiopathy
25
* Hyperplastic Arteriolosclerosis
–Malignant hypertension
26
Medial Calcific Sclerosis
(2)
* Calcification of media
* Does not encroach on vessel lumen
27
Syphilitic Aneurysm
(2)
* Syphilitic aortitis of ascending aorta may
occur in tertiary syphilis
* Obliterative endarteritis of the vasa vasorum
28
Arterial Dissection
* An intimal tear allows dissection of blood
into media - may rupture leading to massive
hemorrhage
29
Arterial Dissection
* Risk factors: (2)
hypertension, connective tissue
abnormality (Marfan Syndrome)
30
Temporal (Giant Cell) Arteritis
(5)
* Most common form of vasculitis in older adults (females over 50y)
* Granulomatous vasculitis
* Flu-like symptoms with muscle and joint pain. ESR elevated
* Branches of carotid artery
* Treatment with corticosteroids
31
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* Branches of carotid artery
(3)
– Headache (temporal artery)
– Visual disturbances (ophthalmic artery) –risk of blindness
– Jaw claudication –pain in masticatory muscles while chewing
32
Polyarteritis Nodosa
(3)
Polyarteritis Nodosa
* Necrotizing arteritis involving multiple organs –lungs spared
* Association with Hepatitis B
* Classical presentation –young adults
33
Polyarteritis Nodosa
* Classical presentation –young adults
(4)
– Hypertension –renal artery involvement
– Abdominal pain with melena –mesenteric artery involvement
– Neurologic disturbances
– Skin lesions
34
Esophageal Varices
(2)
* Cirrhosis of liver causes portal hypertension
* Rupture producing massive upper GI bleed
35
Vasculitis
(2)
* Inflammation of the blood vessel wall
* Etiology unknown –most cases are not infectious
36
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Vasculitis
* Clinical features
(2)
– Systemic - non-specific symptoms of inflammation –fever, fatigue, weight loss, myalgias
– Local - symptoms of organ ischemia due to luminal narrowing or thrombosis
37
* Large vessel vasculitis –
aorta and major
branches
38
* Medium vessel vasculitis –
muscular arteries
that supply organs
39
* Small vessel vasculitis –
arterioles, capillaries,
venules
40
Wegener Granulomatosis
(5)
* Necrotizing granulomatous vasculitis
* Target organs: nasopharynx, lungs, kidneys
* Classic presentation - middle-aged male with:
* “Strawberry” gingiva
* c-ANCA –anti-neutrophil cytoplasmic antibod
41
Wegener Granulomatosis
* Classic presentation - middle-aged male with:
(3)
– Nasopharyngeal ulceration, sinusitis
– Hemoptysis –lung involvement
– Hematuria –renal involvement –glomerulonephritis
42
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Heart Disease
(6)
* Hypertensive Heart Disease
* Heart Failure
* Ischemic Heart Disease
* Valvular Heart Disease
* Infective Endocarditis
* Congenital Heart Disease
43
* Primary hypertension (essential hypertension) –
no identifiable etiology
44
* Secondary hypertension –
identifiable etiology
45
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* Risk factors for hypertension
– Age
– Smoking
– Male gender
– Race - AA > C
– Obesity
– Family history
– Sodium intake
– Ethanol use
– Psychological stress
46
* Optimal blood pressure:
<120 and <80
47
* Normal blood pressure
<130 and <85
48
* Stage I Hypertension
140-159 or 90-99
49
End Organ Damage and
Complications of Hypertension
(5)
* Cardiovascular system
* Peripheral vascular system
* Renal system
* Central nervous system
* Visual system
50
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* Cardiovascular system
(5)
– Accelerated coronary atherosclerosis
– Increased myocardial oxygen demand
– Ventricular remodeling
– Heart failure
– Increased risk for arrhythmias
51
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* Peripheral vascular system
(4)
– Atherosclerosis
– Aortic dissection
– Abdominal aortic aneurysm
– Peripheral vascular disease
52
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* Renal system
(2)
– Hypertensive nephrosclerosis
– End-stage renal disease
53
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* Central nervous system
(2)
– Hemorrhagic CVA
– Thromboembolic CVA
54
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* Visual system
(3)
– Retinal infarction
– Hypertensive retinopathy
– Blindness
55
“Congestive” Heart Failure
(3)
* The final common pathway of many forms of
heart disease
* Inability of the heart to pump a sufficient
amount of blood through the body
* Onset preceded by compensatory
mechanisms (cardiac hypertrophy)
56
What Causes Heart Failure?
(2)
* Systolic dysfunction
* Diastolic dysfunction
57
* Systolic dysfunction -
deterioration of
contractile function
–Ischemic heart disease
58
* Diastolic dysfunction -
inability to relax,
expand and fill
–Left ventricular hypertrophy
59
Cardiac Hypertrophy
* Compensatory mechanism to
(2)
–Pressure overload
–Volume overload
60
Pressure-Overloaded Hypertrophy
(2)
* Concentrically increased wall thickness
* Seen in hypertension, aortic stenosis
61
Volume-Overloaded Hypertrophy
(2)
* Dilation of chambers
* Valvular incompetence
62
Classification of Heart Failure
* Left-sided heart failure -
* Right-sided heart failure -
pulmonary edema
peripheral edema
63
Left-Sided Heart Failure
* Caused by:
(3)
– Ischemic heart disease
– Hypertension
– Valvular disease - aortic and mitral valves
64
Left-Sided Heart Failure
* Clinical effects result from
(2)
– Decreased peripheral blood pressure and flow
– Backup of blood in pulmonary circulation
65
Findings in Left-Sided Heart Failure
(2)
* Pulmonary congestion
* Pulmonary edema
66
Findings in Left-Sided Heart Failure
(3)
* Dyspnea
* Orthopnea
* Paroxysmal nocturnal dyspnea
67
Right-Sided Heart Failure
* Caused by:
(2)
– Left sided heart failure
– Chronic sever pulmonary hypertension
68
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Right-Sided Heart Failure
* Clinical effects result from
(4)
– Hepatic and splenic enlargement
– Peripheral edema
– Pleural effusion
– Ascites
69
Findings in Right-Sided Heart Failure
(4)
* Cor Pulmonale
* Pure right-sided heart failure
* Right ventricular hypertrophy and dilation
* Pulmonary hypertension
70
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Findings in Right-Sided Heart Failure
(6)
* Congestion in systemic and portal venous circulations
* Congestive hepatomegaly - chronic passive congestion
- “nutmeg” liver
* Congestive splenomegaly
* Pleural effusion
* Peripheral edema - pitting edema
* Most common cause of RSHF is LSH
71
Ascites
* May be associated with cardiac, hepatic and
renal disease
72
Ischemic Heart Disease (IHD)
* Result of
* Imbalance between
* Angina pectoris
* Myocardial infarction
coronary artery atherosclerosis
myocardial oxygen
supply and demand
73
Risk of Developing Detectable
Ischemic Heart Disease
(2)
* Number, distribution and structure of
atheromatous plaques
* Degree of narrowing
74
Angina Pectoris
(4)
* Transient myocardial ischemia
* Paroxysmal, recurrent precordial chest
discomfort, constricting, squeezing, choking,
knife-like
* May radiate to: arm, mandible
* Does not produce myocardial necrosis
(infarction)
75
Stable Angina
* Due to a
* Increased demand produces
* Relieved by rest or by
fixed stenosis –an atherosclerotic
plaque reduces coronary perfusion to critical
level
ischemia
nitroglycerin
76
Unstable Angina
* Due to a
* Frequently occurs at
* Medical emergency -
may evolve into
complicated
plaque –a variable
stenosis
rest
MI
77
Variant Angina –Prinzmetal Angina
(4)
* Coronary arterial spasm secondary to
vascular hyper-reactivity
* Occurs at rest
* May be unassociated with ASCAD
* Cocaine users -> vasospasm
78
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Pathogenesis of Transmural Acute
Myocardial Infarction
major risk factor
(6)
* Coronary atherosclerosis
* Complicated plaque
* Platelet adhesion and activation
* Thrombus formation
* Vessel occlusion
* Myocardial infarction (cellular necrosis)
79
Serum Cardiac Markers
(2)
* Cardiac-specific Troponin (T or I)
* Creatine phosphokinase (MB fraction) –CPK-
MB
80
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Post-MI Complications
* Contractile dysfunction
* Arrhythmias
* Myocardial rupture
* Pericarditis
* Right ventricular infarction
* Infarct extension (new)
* Infarct extension (dilatation)
* Mural thrombus
* Ventricular aneurysm
* Papillary muscle dysfunction
* Progressive late heart failure
81
Valvular Heart Disease
(3)
* Stenosis - doesn’t open completely (impedes
forward flow)
* Insufficiency/incompetence - doesn’t close
completely
(allows reverse flow)
* Abnormalities of flow produce murmurs
82
Valvular Heart Disease
* Abnormalities of
flow produce murmurs
83
Major Valvular Lesions
(4)
* Aortic stenosis
* Aortic insufficiency
* Mitral stenosis –
rheumatic heart disease
* Mitral insufficiency - myxomatous
degeneration (mitral valve prolapse)
84
Acute Rheumatic Fever
(4)
* Acute rheumatic fever is a complication of
Group A streptococcal pharyngitis
* Antibodies cross react with cardiac antigens
* Inflammation leads to fibrotic valvular
disease
* Type II Hypersensitivity Reaction
85
Rheumatic Heart Disease
(4)
* Pericardium - fibrinous pericarditis
* Myocardium - myocarditis
* Valves
* ARF is the most frequent cause of mitral stenosis
86
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* Valves
(3)
– Mitral vegetations
– Thickened leaflets
– Fused commissures
87
Infective Endocarditis
* Most frequently ---
* --- of organism determines course
* --- formation on damaged endothelium (vegetations)
* Bacteremia results in microbial colonization of ---
* --- emboli
bacterial
Virulence
Thrombus
vegetations
Septic
88
* Most frequently bacterial
(2)
– Strep viridans
– Staph aureus –IV drug abusers
89
Infective Endocarditis
(3)
* Left side of heart affected most commonly
(aortic valve)
* Right side –for IV drug abusers
* Mortality due to heart failure
90
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Cardiac Conditions Requiring Antibiotic
Prophylaxis for Infective Endocarditis
1. Prosthetic cardiac valves, including transcatheter-implanted prostheses and
homografts.
2. Prosthetic material used for heart valve repair, such as annuloplasty rings, chords
or clips.
3. Previous IE.
4. Unrepaired cyanotic congenital heart defect (birth defects with oxygen levels
lower than normal) or repaired congenital heart defect, with residual shunts or
valvular regurgitation at the site adjacent to the site of a prosthetic patch or
prosthetic device.
5. Cardiac transplant with valve regurgitation due to a structurally abnormal valve.
* Except for the conditions listed above, antibiotic prophylaxis is no longer recommended for any other
form of congenital heart disease.
91
Congenital Heart Disease
* Abnormalities of the
* Faulty embryogenesis - weeks
* Susceptibility to
heart and great vessels
3 to 8
infective endocarditis –
antimicrobial prophylaxis
92
Etiology of Congenital Heart Disease
(3)
* Most have no identifiable cause - multifactorial environmental, genetic and maternal factors
* Environmental
* Genetic
93
Etiology of Congenital Heart Disease
* Environmental
(2)
– Infectious - fetal rubella or cytomegalovirus infection
– Drugs –accutane, lithium, anti-seizure medications, cocaine, alcohol
94
Etiology of Congenital Heart Disease
* Genetic
(2)
– Trisomy 21
– Turner syndrome
95
Categories of Congenital Heart
Disease
* Malformations causing:
(3)
* Malformations causing: Left-to-Right Shunts
* Malformations causing: Right-to-Left Shunts
* Malformations causing Obstructions
96
Right-to-Left Shunts
(2)
* Pulmonary blood flow is decreased, allowing
poorly-oxygenated blood to enter the
systemic circulation
* Cyanotic Congenital Heart Disease
97
Right-to-Left Shunts
* May be associated with paradoxical
embolism –
a septal defect allows venous
emboli to bypass the lungs and enter
systemic arterial circulation
98
Tetralogy of Fallot
(2)
* Right-to-Left Shunt
* Most common form of cyanotic congential heart disease
99
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Tetralogy of Fallot
(4)
1. Ventricular septal defect (VSD)
2. Sub-pulmonary stenosis
3. Right ventricular hypertrophy
4. Aorta overrides VSD
100
* --- is most common form of Congenital Heart Disease
VSD
101
* --- is most common form of CYANOTIC Congenital Heart Disease
TOF
102
Transposition of the Great Arteries
(5)
* Separate systemic and pulmonary circulations is incompatible with post-natal life and requires shunt for survival
* Stable shunt
* Unstable shunts
* RV hypertrophy
* LV atrophy
103
* Stable shunt (1)
* Unstable shunts (2)
– Ventricular Septal Defect
– Patent Foramen Ovale
– Patent Ductus Arteriosus
104
Left-to-Right Shunts
(2)
* Pulmonary blood flow increased
–Pulmonary hypertension
105
Left-to-Right Shunts
(4)
* Ventricular Septal Defect
* Atrial Septal Defect
* Atrial-Ventricular Septal Defect
* Patent Ductus Arteriosus
106
Patent Ductus Arteriosus
(4)
* The ductus arteriosus is a normal fetal blood
vessel that allows blood to bypass the lungs
* PDA is a left-to-right shunt from the aorta to
the pulmonary artery
* When pulmonary hypertension develops,
shunt reverses and cyanosis develops
107
Coarctation of the Aorta
(2)
* Obstructive defect located in the area of the
ductus that may be asymptomatic until
adulthood
* Rib notching due to collateral circulation
108
Coarctation of the Aorta
* Hypertension --- to coarctation
* Hypotension --- to coarctation
proximal
distal
