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Pathology > Blood Vessels and Cardiovascular System Pathology > Flashcards

Blood Vessels and Cardiovascular System Pathology Flashcards

1
Q

Cardiovascular System
(3)

A

*Blood vessels
*Heart
*(Blood)

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2
Q

Mechanism of Vascular Disease
(3)

A
  • Narrowing of lumen
  • Obstruction of lumen
  • Weakening of wall
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3
Q
  • Narrowing of lumen
    (1)
A

–Athersclerosis

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4
Q
  • Obstruction of lumen
    (2)
A

–Thrombus
–Embolus

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5
Q
  • Weakening of wall
    (2)
A

–Dilation
–Rupture

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6
Q

Arteriosclerosis
* Three patterns of arteriosclerosis
(3)

A

–Atherosclerosis
* Atheromas
–Arteriolosclerosis
–Medial Calcific Sclerosis

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7
Q

Constitutional risk
factors (non-modifiable)
(4)

A

– Age
– Gender
– Family history
– Genetic abnormalities

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8
Q

Major risk factors (modifiable)
(4)

A

– Hyperlipidemia
– Hypertension
– Cigarette smoking
– Diabetes mellitus

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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)
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10
Q
  • Low Density Lipoprotein (< 100 mg/dl)
    (2)
A

– “Bad cholesterol”
– Delivers cholesterol to peripheral tissues

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11
Q
  • High Density Lipoprotein (> 40 mg/dl)
    (2)
A

– “Good cholesterol”
– Mobilizes cholesterol from atheromas and transports it to the liver for excretion

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12
Q

skipped
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)

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13
Q

Atherosclerosis

A
  • Atheromatous plaques project into and
    obstruct the lumen and weaken the media
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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
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15
Q

skipped
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
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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
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17
Q

Fatty Streak
(2)

A
  • Earliest lesion of atherosclerosis
  • Lipid filled foam cells within the intima
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18
Q

Atheroma

A
  • Plague like lesion that begins in the intima
    and impinges on lumen
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19
Q

Complicated Plaque

A
  • Ulceration exposes thrombogenic material
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20
Q

Complications of Atheromas
(6)

A
  1. Ischemic injury - compromised blood flow to distal organs
  2. Disruption –exposes thrombogenic substances
  3. Thrombosis - clotting on surface of ulcerated plaque causes
    further narrowing
  4. Embolization –thrombus or plaque material may embolize
    (thromboembolus)
  5. Hemorrhage –a hematoma may expand or rupture plaque
  6. Aneurysm - weak wall may dilate and rupture
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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
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22
Q

Atherosclerosis

A
  • Atheromatous plaques project into and
    obstruct the lumen and weaken the media
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23
Q

Arteriolosclerosis
(4)

A
  • Hypertension
  • Small blood vessel disease
  • Hyaline Arteriolosclerosis
  • Hyperplastic Arteriolosclerosis
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24
Q
  • Hyaline Arteriolosclerosis
A

–Diabetic microangiopathy

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25
Q
  • Hyperplastic Arteriolosclerosis
A

–Malignant hypertension

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26
Q

Medial Calcific Sclerosis
(2)

A
  • Calcification of media
  • Does not encroach on vessel lumen
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27
Q

Syphilitic Aneurysm
(2)

A
  • Syphilitic aortitis of ascending aorta may
    occur in tertiary syphilis
  • Obliterative endarteritis of the vasa vasorum
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28
Q

Arterial Dissection

A
  • An intimal tear allows dissection of blood
    into media - may rupture leading to massive
    hemorrhage
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29
Q

Arterial Dissection
* Risk factors: (2)

A

hypertension, connective tissue
abnormality (Marfan Syndrome)

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30
Q

Temporal (Giant Cell) Arteritis
(5)

A
  • 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
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31
Q

skipped
* Branches of carotid artery
(3)

A

– Headache (temporal artery)
– Visual disturbances (ophthalmic artery) –risk of blindness
– Jaw claudication –pain in masticatory muscles while chewing

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32
Q

Polyarteritis Nodosa
(3)

A

Polyarteritis Nodosa
* Necrotizing arteritis involving multiple organs –lungs spared
* Association with Hepatitis B
* Classical presentation –young adults

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33
Q

Polyarteritis Nodosa
* Classical presentation –young adults
(4)

A

– Hypertension –renal artery involvement
– Abdominal pain with melena –mesenteric artery involvement
– Neurologic disturbances
– Skin lesions

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34
Q

Esophageal Varices
(2)

A
  • Cirrhosis of liver causes portal hypertension
  • Rupture producing massive upper GI bleed
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35
Q

Vasculitis
(2)

A
  • Inflammation of the blood vessel wall
  • Etiology unknown –most cases are not infectious
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36
Q

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Vasculitis
* Clinical features
(2)

A

– Systemic - non-specific symptoms of inflammation –fever, fatigue, weight loss, myalgias
– Local - symptoms of organ ischemia due to luminal narrowing or thrombosis

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37
Q
  • Large vessel vasculitis –
A

aorta and major
branches

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38
Q
  • Medium vessel vasculitis –
A

muscular arteries
that supply organs

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39
Q
  • Small vessel vasculitis –
A

arterioles, capillaries,
venules

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40
Q

Wegener Granulomatosis
(5)

A
  • Necrotizing granulomatous vasculitis
  • Target organs: nasopharynx, lungs, kidneys
  • Classic presentation - middle-aged male with:
  • “Strawberry” gingiva
  • c-ANCA –anti-neutrophil cytoplasmic antibod
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41
Q

Wegener Granulomatosis
* Classic presentation - middle-aged male with:
(3)

A

– Nasopharyngeal ulceration, sinusitis
– Hemoptysis –lung involvement
– Hematuria –renal involvement –glomerulonephritis

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42
Q

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Heart Disease
(6)

A
  • Hypertensive Heart Disease
  • Heart Failure
  • Ischemic Heart Disease
  • Valvular Heart Disease
  • Infective Endocarditis
  • Congenital Heart Disease
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43
Q
  • Primary hypertension (essential hypertension) –
A

no identifiable etiology

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44
Q
  • Secondary hypertension –
A

identifiable etiology

45
Q

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* Risk factors for hypertension

A

– Age
– Smoking
– Male gender
– Race - AA > C
– Obesity
– Family history
– Sodium intake
– Ethanol use
– Psychological stress

46
Q
  • Optimal blood pressure:
A

<120 and <80

47
Q
  • Normal blood pressure
A

<130 and <85

48
Q
  • Stage I Hypertension
A

140-159 or 90-99

49
Q

End Organ Damage and
Complications of Hypertension
(5)

A
  • Cardiovascular system
  • Peripheral vascular system
  • Renal system
  • Central nervous system
  • Visual system
50
Q

skipped
* Cardiovascular system
(5)

A

– Accelerated coronary atherosclerosis
– Increased myocardial oxygen demand
– Ventricular remodeling
– Heart failure
– Increased risk for arrhythmias

51
Q

skipped
* Peripheral vascular system
(4)

A

– Atherosclerosis
– Aortic dissection
– Abdominal aortic aneurysm
– Peripheral vascular disease

52
Q

skipped
* Renal system
(2)

A

– Hypertensive nephrosclerosis
– End-stage renal disease

53
Q

skipped
* Central nervous system
(2)

A

– Hemorrhagic CVA
– Thromboembolic CVA

54
Q

skipped
* Visual system
(3)

A

– Retinal infarction
– Hypertensive retinopathy
– Blindness

55
Q

“Congestive” Heart Failure
(3)

A
  • 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
Q

What Causes Heart Failure?
(2)

A
  • Systolic dysfunction
  • Diastolic dysfunction
57
Q
  • Systolic dysfunction -
A

deterioration of
contractile function
–Ischemic heart disease

58
Q
  • Diastolic dysfunction -
A

inability to relax,
expand and fill
–Left ventricular hypertrophy

59
Q

Cardiac Hypertrophy
* Compensatory mechanism to
(2)

A

–Pressure overload
–Volume overload

60
Q

Pressure-Overloaded Hypertrophy
(2)

A
  • Concentrically increased wall thickness
  • Seen in hypertension, aortic stenosis
61
Q

Volume-Overloaded Hypertrophy
(2)

A
  • Dilation of chambers
  • Valvular incompetence
62
Q

Classification of Heart Failure
* Left-sided heart failure -
* Right-sided heart failure -

A

pulmonary edema
peripheral edema

63
Q

Left-Sided Heart Failure
* Caused by:
(3)

A

– Ischemic heart disease
– Hypertension
– Valvular disease - aortic and mitral valves

64
Q

Left-Sided Heart Failure
* Clinical effects result from
(2)

A

– Decreased peripheral blood pressure and flow
– Backup of blood in pulmonary circulation

65
Q

Findings in Left-Sided Heart Failure
(2)

A
  • Pulmonary congestion
  • Pulmonary edema
66
Q

Findings in Left-Sided Heart Failure
(3)

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
67
Q

Right-Sided Heart Failure
* Caused by:
(2)

A

– Left sided heart failure
– Chronic sever pulmonary hypertension

68
Q

skipped
Right-Sided Heart Failure
* Clinical effects result from
(4)

A

– Hepatic and splenic enlargement
– Peripheral edema
– Pleural effusion
– Ascites

69
Q

Findings in Right-Sided Heart Failure
(4)

A
  • Cor Pulmonale
  • Pure right-sided heart failure
  • Right ventricular hypertrophy and dilation
  • Pulmonary hypertension
70
Q

skipped
Findings in Right-Sided Heart Failure
(6)

A
  • 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
Q

Ascites

A
  • May be associated with cardiac, hepatic and
    renal disease
72
Q

Ischemic Heart Disease (IHD)
* Result of
* Imbalance between
* Angina pectoris
* Myocardial infarction

A

coronary artery atherosclerosis
myocardial oxygen
supply and demand

73
Q

Risk of Developing Detectable
Ischemic Heart Disease
(2)

A
  • Number, distribution and structure of
    atheromatous plaques
  • Degree of narrowing
74
Q

Angina Pectoris
(4)

A
  • 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
Q

Stable Angina
* Due to a
* Increased demand produces
* Relieved by rest or by

A

fixed stenosis –an atherosclerotic
plaque reduces coronary perfusion to critical
level
ischemia
nitroglycerin

76
Q

Unstable Angina
* Due to a
* Frequently occurs at
* Medical emergency -
may evolve into

A

complicated
plaque –a variable
stenosis
rest
MI

77
Q

Variant Angina –Prinzmetal Angina
(4)

A
  • Coronary arterial spasm secondary to
    vascular hyper-reactivity
  • Occurs at rest
  • May be unassociated with ASCAD
  • Cocaine users -> vasospasm
78
Q

skipped
Pathogenesis of Transmural Acute
Myocardial Infarction
major risk factor

(6)

A
  • Coronary atherosclerosis
  • Complicated plaque
  • Platelet adhesion and activation
  • Thrombus formation
  • Vessel occlusion
  • Myocardial infarction (cellular necrosis)
79
Q

Serum Cardiac Markers
(2)

A
  • Cardiac-specific Troponin (T or I)
  • Creatine phosphokinase (MB fraction) –CPK-
    MB
80
Q

skipped
Post-MI Complications

A
  • 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
Q

Valvular Heart Disease
(3)

A
  • Stenosis - doesn’t open completely (impedes
    forward flow)
  • Insufficiency/incompetence - doesn’t close
    completely
    (allows reverse flow)
  • Abnormalities of flow produce murmurs
82
Q

Valvular Heart Disease
* Abnormalities of

A

flow produce murmurs

83
Q

Major Valvular Lesions
(4)

A
  • Aortic stenosis
  • Aortic insufficiency
  • Mitral stenosis –
    rheumatic heart disease
  • Mitral insufficiency - myxomatous
    degeneration (mitral valve prolapse)
84
Q

Acute Rheumatic Fever
(4)

A
  • 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
Q

Rheumatic Heart Disease
(4)

A
  • Pericardium - fibrinous pericarditis
  • Myocardium - myocarditis
  • Valves
  • ARF is the most frequent cause of mitral stenosis
86
Q

skipped
* Valves
(3)

A

– Mitral vegetations
– Thickened leaflets
– Fused commissures

87
Q

Infective Endocarditis
* Most frequently —
* — of organism determines course
* — formation on damaged endothelium (vegetations)
* Bacteremia results in microbial colonization of —
* — emboli

A

bacterial
Virulence
Thrombus
vegetations
Septic

88
Q
  • Most frequently bacterial
    (2)
A

– Strep viridans
– Staph aureus –IV drug abusers

89
Q

Infective Endocarditis
(3)

A
  • Left side of heart affected most commonly
    (aortic valve)
  • Right side –for IV drug abusers
  • Mortality due to heart failure
90
Q

skipped
Cardiac Conditions Requiring Antibiotic
Prophylaxis for Infective Endocarditis

A
  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
Q

Congenital Heart Disease
* Abnormalities of the
* Faulty embryogenesis - weeks
* Susceptibility to

A

heart and great vessels
3 to 8
infective endocarditis –
antimicrobial prophylaxis

92
Q

Etiology of Congenital Heart Disease
(3)

A
  • Most have no identifiable cause - multifactorial environmental, genetic and maternal factors
  • Environmental
  • Genetic
93
Q

Etiology of Congenital Heart Disease
* Environmental
(2)

A

– Infectious - fetal rubella or cytomegalovirus infection
– Drugs –accutane, lithium, anti-seizure medications, cocaine, alcohol

94
Q

Etiology of Congenital Heart Disease
* Genetic
(2)

A

– Trisomy 21
– Turner syndrome

95
Q

Categories of Congenital Heart
Disease
* Malformations causing:
(3)

A
  • Malformations causing: Left-to-Right Shunts
  • Malformations causing: Right-to-Left Shunts
  • Malformations causing Obstructions
96
Q

Right-to-Left Shunts
(2)

A
  • Pulmonary blood flow is decreased, allowing
    poorly-oxygenated blood to enter the
    systemic circulation
  • Cyanotic Congenital Heart Disease
97
Q

Right-to-Left Shunts
* May be associated with paradoxical
embolism –

A

a septal defect allows venous
emboli to bypass the lungs and enter
systemic arterial circulation

98
Q

Tetralogy of Fallot
(2)

A
  • Right-to-Left Shunt
  • Most common form of cyanotic congential heart disease
99
Q

skipped
Tetralogy of Fallot
(4)

A
  1. Ventricular septal defect (VSD)
  2. Sub-pulmonary stenosis
  3. Right ventricular hypertrophy
  4. Aorta overrides VSD
100
Q
  • — is most common form of Congenital Heart Disease
101
Q
  • — is most common form of CYANOTIC Congenital Heart Disease
102
Q

Transposition of the Great Arteries
(5)

A
  • 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
Q
  • Stable shunt (1)
  • Unstable shunts (2)
A

– Ventricular Septal Defect

– Patent Foramen Ovale
– Patent Ductus Arteriosus

104
Q

Left-to-Right Shunts
(2)

A
  • Pulmonary blood flow increased
    –Pulmonary hypertension
105
Q

Left-to-Right Shunts
(4)

A
  • Ventricular Septal Defect
  • Atrial Septal Defect
  • Atrial-Ventricular Septal Defect
  • Patent Ductus Arteriosus
106
Q

Patent Ductus Arteriosus
(4)

A
  • 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
Q

Coarctation of the Aorta
(2)

A
  • Obstructive defect located in the area of the
    ductus that may be asymptomatic until
    adulthood
  • Rib notching due to collateral circulation
108
Q

Coarctation of the Aorta
* Hypertension — to coarctation
* Hypotension — to coarctation

A

proximal
distal

Pathology (23 decks)

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