Blood Vessels and CVS Flashcards

1
Q

What are the Three patterns of arteriosclerosis?

A
  1. Atherosclerosis
  2. Medial Calcific Sclerosis
  3. Arteriolosclerosis
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2
Q

• Atheromatous plaques project
into and obstruct the lumen
and weaken the media

A

Atherosclerosis

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3
Q
• 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
A

Atherosclerosis

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4
Q
  • Calcification of media

* Does not encroach on vessel lumen

A

MEdial calcific sclerosis

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5
Q
• Affects arterioles
• Thickened walls reduce lumen 
diameter causing ischemic injury
• Hyaline arteriolosclerosis
– Benign hypertension
– Diabetes mellitus
• Hyperplastic arteriolosclerosis
– Malignant hypertension 
(200/120 mm Hg)
• Ischemia: reduced blood flow
• Hypoxia: deficiency of oxygen
• Infarct: complete loss of blood supply 
causes localized area of necrosis
A

Arteriosclerosis

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6
Q

What are the 3 Stages in the Progression of Atherosclerosis in order?

A
  1. Fatty streak
  2. Atheroma (plaque): covered by fibrous
    cap
  3. Complicated plaque: ulcerated
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7
Q

Lipid-filled foam cells (macrophages) within

the intima

A

Fatty streak

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8
Q

Plaque-like lesion that begins
in the intima and impinges on
the vessel lumen

A

Atheroma

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9
Q
Complications of \_\_\_\_\_\_:
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
A

Atheromas

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10
Q
Major Clinical Consequences of \_\_\_\_\_\_\_
• Myocardial infarct: Heart attack
• Cerebral infarct: Stroke
• Aortic aneurysm: Rupture
• Peripheral vascular disease: 
Gangrene of legs
A

Atherosclerosis

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11
Q

Risk Factors for _______
Constitutional (non-modifiable) risk factors
– Age– Gender– Family history– Genetic abnormalities
Major (modifiable) risk factors
– Hyperlipidemia– Hypertension– Cigarette smoking– Diabetes mellitus

  • Multiple risk factors
    multiplies risk
    Additional risk factors
    – Obesity– Physical activity– Personality type– Alcohol– Trans fatty acids– Lipoprotein A – Hyperhomocystinemia– Systemic inflammatory state (C-reactive protein CRP)
A

Atherosclerosis

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12
Q
• Total Cholesterol < 200 mg/dl
• Low Density Lipoprotein < 100 mg/dl
– “Bad cholesterol”
– Delivers cholesterol to peripheral 
tissues
• High Density Lipoprotein > 40 mg/dl
– “Good cholesterol”
– Mobilizes cholesterol from atheromas
and transports it to the liver for 
excretion
A

Hyperlipidemia

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13
Q
  • Syphilitic aortitis of ascending aorta may occur in tertiary syphilis
  • Obliterative endarteritis of the vasa vasorum
A

Syphilitic Aneurysm

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14
Q

• An intimal tear allows dissection of blood into media: may rupture leading to massive
hemorrhage
• Risk factors: hypertension, connective tissue abnormality (Marfan Syndrome)

A

Arteria dissection

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15
Q

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

A

Esophageal Varices

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16
Q

• Prolonged increased intraluminal pressure and loss of vessel wall support produces dilated, tortuous veins
valvular incompetence
• Venous stasis - congestion, edema, pain,

A

Varicose veins

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17
Q
  • Lymphatic spread of bacterial infection

* Painful red streaks and regional lymphadenopathy

A

Lymphangitis

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18
Q
• Compression of 
superior vena 
cava by 
neoplasm 
obstructing 
venous return
A

Superior vena cava syndrome

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19
Q

• Inflammation of the blood vessel wall
• Etiology unknown: most cases are not infectious
• Clinical features
– Systemic : non-specific symptoms of inflammation
• Fever, fatigue, weight loss, myalgias
– Local : symptoms of organ ischemia due to luminal narrowing or thrombosis

A

Vasculitis

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20
Q
• 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
– Headache 
– Visual disturbances 50%
– Jaw claudication
• Treatment: Anti-inflammatory
– Corticosteroids
A

Large Vessel Vasculitis: Temporal (Giant Cell) Arteritis

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21
Q
• Necrotizing arteritis involving multiple organs: lungs spared
• Association with Hepatitis B
• Classical presentation : young adults
– Hypertension: Renal artery involvement
– Abdominal pain with GI bleeding:
• mesenteric artery involvement
– Neurologic disturbances
– Skin lesions
A

Medium Vessel Vasculitis: Polyarteritis Nodosa

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22
Q
• Necrotizing granulomatous 
vasculitis
• Target organs: Nasopharynx, lungs, 
kidneys
– Nasopharyngeal ulceration, 
sinusitis 
– Hemoptysis: Lung involvement
– Hematuria: Renal involvement
• Glomerulonephritis
– ^ Middle-aged males
• “Strawberry” gingiva
• Antiproteinase-3 (PR3)
• c-ANCA 95%
A

Small Vessel Vasculitis: Wegener Granulomatosis

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23
Q

• Optimal blood pressure:

A

<120 and <80

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24
Q

• Normal blood pressure

A

<130 and <85

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25
• Stage I Hypertension
140-159 or 90-99
26
``` • 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) ```
CHF
27
Left-sided heart failure: _____ edema
pulmonary | edema
28
Right-sided heart failure: _____ edema
peripheral | edema
29
______ dysfunction: Deterioration of contractile function – Ischemic heart disease – Hypertension
Systolic
30
______ dysfunction: Inability to relax, expand and fill – Left ventricular hypertrophy
Diastolic
31
______ hypertrophy • Concentrically increased wall thickness • Seen in hypertension, aortic stenosis Normal LV < 1.5 cm
Pressure-Overloaded Hypertrophy
32
_____ hypertrophy • Dilation of chambers • Valvular incompetence
Volume-Overloaded Hypertrophy
33
``` • Caused by: – Ischemic heart disease – Hypertension – Valvular disease: aortic and mitral valves • Clinical effects result from – Decreased peripheral blood pressure and flow – Backup of blood in pulmonary circulation • Pulmonary congestion • Pulmonary edema ```
Left sided heart failure
34
• Dyspnea : Shortness of breath • Orthopnea: Difficulty breathing when lying flat • Paroxysmal nocturnal dyspnea: Awakened by severe shortness of breath and relieved by sitting up
Left sided heart failure
35
* Pure right-sided heart failure * Right ventricular hypertrophy and dilation * Pulmonary hypertension
Cor pulmonale
36
``` • 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 right-sided heart failure is left-sided heart failure ```
Right sided heart failure
37
``` • Result of coronary artery atherosclerosis • Imbalance between myocardial oxygen supply and demand  Angina pectoris  Myocardial infarction ```
Ischemic heart diesease
38
Does primary or secondary hypertension have an identifiable etiology?
Secondary
39
• Compensatory mechanism to – Pressure overload – Volume overload
Cardiac hypertrophy
40
``` • Transient myocardial ischemia • Paroxysmal, recurrent pericardial chest discomfort, constricting, squeezing, choking, knife-like • May radiate to arm, mandible • Does not produce myocardial necrosis (infarction) ```
Angina pectoris
41
``` • Due to a fixed stenosis: an atherosclerotic plaque reduces coronary perfusion to critical level • Increased demand produces ischemia • Pain that is predictably reproducible & consistent over time • Precipitated by physical effort such as walking or climbing stairs but may also occur with eating or stress. • Pain is relieved by cessation of the precipitating activity, by rest, or by the use of nitroglycerin ```
Stable angina
42
``` • Due to a complicated plaque: a variable stenosis • New onset of pain • Pain that is increasing in frequency, more intense than before – Key feature is the changing character or pattern of the pain. • Pain that is precipitated by less effort than before, or pain that occurs at rest • Not readily relieved by nitroglycerin • Medical emergency: May evolve into MI ```
Unstable angina
43
``` • Coronary arterial spasm secondary to vascular hyper-reactivity • Occurs at rest • May be unassociated with atherosclerosis and coronary artery disease • Cocaine users -> vasospasm ```
Variant Angina (Prinzmetal Angina)
44
``` Pathogenesis of ___________ • Coronary atherosclerosis • Complicated plaque • Platelet adhesion and activation • Thrombus formation • Vessel occlusion • Myocardial infarction (cellular necrosis) ```
Transmural Acute Myocardial Infarction
45
What are the 3 serum cardiac markers?
* Myoglobin * Cardiac-specific Troponin (T or I) * Creatine kinase (MB fraction): CK-MB
46
* Aneurysm * Wall rupture * Mural thrombus * Papillary muscle rupture
Post MI complications
47
``` ________ diseases • Stenosis: Doesn’t open completely – Impedes forward flow • Insufficiency/incompetence: Doesn’t close completely – Allows reverse flow Abnormalities of flow produce murmurs ```
Valvular heart diseases
48
``` • Aortic stenosis • Aortic insufficiency • Mitral stenosis – rheumatic heart disease • Mitral insufficiency - myxomatous degeneration (mitral valve prolapse) ```
Major valvular lesions
49
• Acute rheumatic fever is a complication of Group A streptococcal pharyngitis • Antibodies to Strep cross react with cardiac antigens • Inflammation leads to fibrotic valvular disease Type II Hypersensitivity Reaction
Acute rheumatic fever
50
The following molecules are associated with _______: • Anitchkow cells (macrophages) • Aschoff body
Acute Rheumatic fever
51
``` • Pericardium: fibrinous pericarditis • Myocardium - myocarditis • Valves – Mitral vegetations – Thickened leaflets – Fused commissures • ARF is the most frequent cause of mitral stenosis ```
Rheumatic heart disease
52
``` • Most frequently bacterial – Strep viridans (50-60%) – Staph aureus: IV drug abusers • Virulence of organism determines course • Thrombus formation on damaged endothelium (vegetations) • Bacteremia results in microbial colonization of vegetations • Septic emboli ```
Infective endocarditis
53
• Left side of heart affected most commonly (aortic valve) • Right side: for IV drug abusers • Mortality due to heart failure
Infective endocarditis
54
Prevention of ________: • Antibiotic prophylaxis for procedures causing bacteremia: dental, gastrointestinal, genitourinary, upper respiratory tract • Dental procedures that involve manipulation of gingival tissue, manipulation of the periapical region of teeth, or perforation of the oral mucosa
Infective endocarditis
55
``` • Abnormalities of the heart and great vessels that are present at birth • = 20-30% of all birth defects • Faulty embryogenesis: weeks 3 to 8 • Most cases: – Atrioventricular, ventricular or atrial septal defect – Pulmonary stenosis – Patent ductus arteriosus – Tetralogy of Fallot – Coarctation of aorta – Aortic stenosis – Transposition of great arteries • 90% have no identifiable cause ``` Susceptibility to infective endocarditis: antimicrobial prophylaxis
Congenital Heart Disease
56
``` Etiology of ______" • Most have no identifiable cause: multifactorial environmental, genetic and maternal factors • Genetic – Trisomy 21 – Turner syndrome • Environmental – Infectious • fetal rubella or cytomegalovirus infection – Drugs • accutane, lithium, anti- seizure medications, cocaine, alcohol ```
Congenital heart disease
57
• Malformations causing Right-to-Left Shunts: _________
Cyanosis
58
• Malformations causing Left-to-Right Shunts: ________
– Most common
59
``` _______ shunts: • Pulmonary blood flow is decreased poorly-oxygenated blood enters the systemic circulation • Cyanotic Congenital Heart Disease • May be associated with paradoxical embolism – Septal defect allows venous emboli to bypass the lungs and enter systemic arterial circulation • Begin with “T” – Tetralogy of Fallot – Transposition of the Great Vessels ```
Right to left shunts
60
``` • Most common form of cyanotic congenital heart disease • Right-to-Left Shunt 1. Ventricular septal defect (VSD) : most common form of congenital Heart Disease 2. Sub-pulmonary stenosis 3. Right ventricular hypertrophy 4. Aorta overides VSD ```
Tetralogy of fallot
61
``` ________ Shunts • Most common • Pulmonary blood flow increased – Pulmonary hypertension – Shunt reversal -> cyanosis (Eisenmenger syndrome) All contain a “D” • Ventricular Septal Defect • Atrial Septal Defect • Atrial-Ventricular Septal Defect • Patent Ductus Arteriosus ```
Left-to-Right Shunts
62
``` • Normal fetal blood vessel that allows blood to bypass the lungs • Left-to-right shunt from the aorta to the pulmonary artery • When pulmonary hypertension develops, shunt reverses and cyanosis develops – (Eisenmenger syndrome) ```
Patent Ductus Arteriosus: Connects Pulmonary Artery and Aorta
63
``` • Obstructive defect located in the area of the ductus that may be asymptomatic until adulthood • Rib notching due to collateral circulation • Males 2:1 ```
Coarctation of the Aorta
64
Is there hypo or hypertension proximal to coarction?
Hypertension
65
Is there hypo or hypertension distal to coarction?
Hypotension