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
Q

• Stage I Hypertension

A

140-159 or 90-99

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26
Q
• 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)
A

CHF

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27
Q

Left-sided heart failure: _____ edema

A

pulmonary

edema

28
Q

Right-sided heart failure: _____ edema

A

peripheral

edema

29
Q

______ dysfunction: Deterioration of
contractile function
– Ischemic heart disease
– Hypertension

A

Systolic

30
Q

______ dysfunction: Inability to
relax, expand and fill
– Left ventricular hypertrophy

A

Diastolic

31
Q

______ hypertrophy
• Concentrically increased wall thickness
• Seen in hypertension, aortic stenosis
Normal LV < 1.5 cm

A

Pressure-Overloaded Hypertrophy

32
Q

_____ hypertrophy
• Dilation of chambers
• Valvular incompetence

A

Volume-Overloaded Hypertrophy

33
Q
• 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
A

Left sided heart failure

34
Q

• Dyspnea : Shortness of breath
• Orthopnea: Difficulty breathing when lying flat
• Paroxysmal nocturnal dyspnea: Awakened by severe shortness
of breath and relieved by sitting up

A

Left sided heart failure

35
Q
  • Pure right-sided heart failure
  • Right ventricular hypertrophy and dilation
  • Pulmonary hypertension
A

Cor pulmonale

36
Q
• 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
A

Right sided heart failure

37
Q
• Result of coronary artery 
atherosclerosis
• Imbalance between  myocardial 
oxygen supply and demand
 Angina pectoris
 Myocardial infarction
A

Ischemic heart diesease

38
Q

Does primary or secondary hypertension have an identifiable etiology?

A

Secondary

39
Q

• Compensatory mechanism to
– Pressure overload
– Volume overload

A

Cardiac hypertrophy

40
Q
• Transient myocardial ischemia
• Paroxysmal, recurrent pericardial 
chest discomfort, constricting, 
squeezing, choking, knife-like
• May radiate to arm, mandible
• Does not produce myocardial 
necrosis (infarction)
A

Angina pectoris

41
Q
• 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
A

Stable angina

42
Q
• 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
A

Unstable angina

43
Q
• Coronary arterial spasm secondary to 
vascular hyper-reactivity
• Occurs at rest
• May be unassociated with 
atherosclerosis and coronary artery 
disease
• Cocaine users -> vasospasm
A

Variant Angina (Prinzmetal Angina)

44
Q
Pathogenesis of \_\_\_\_\_\_\_\_\_\_\_
• Coronary atherosclerosis
• Complicated plaque
• Platelet adhesion and activation
• Thrombus formation
• Vessel occlusion
• Myocardial infarction (cellular 
necrosis)
A

Transmural Acute Myocardial Infarction

45
Q

What are the 3 serum cardiac markers?

A
  • Myoglobin
  • Cardiac-specific Troponin (T or I)
  • Creatine kinase (MB fraction): CK-MB
46
Q
  • Aneurysm
  • Wall rupture
  • Mural thrombus
  • Papillary muscle rupture
A

Post MI complications

47
Q
\_\_\_\_\_\_\_\_ diseases
• Stenosis: Doesn’t open completely
– Impedes forward flow
• Insufficiency/incompetence: Doesn’t close completely 
– Allows reverse flow
Abnormalities of flow produce murmurs
A

Valvular heart diseases

48
Q
• Aortic stenosis
• Aortic insufficiency
• Mitral stenosis –
rheumatic heart disease
• Mitral insufficiency -
myxomatous degeneration 
(mitral valve prolapse)
A

Major valvular lesions

49
Q

• 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

A

Acute rheumatic fever

50
Q

The following molecules are associated with _______:
• Anitchkow cells (macrophages)
• Aschoff body

A

Acute Rheumatic fever

51
Q
• Pericardium: fibrinous pericarditis
• Myocardium - myocarditis
• Valves 
– Mitral vegetations
– Thickened leaflets
– Fused commissures
• ARF is the most frequent cause of 
mitral stenosis
A

Rheumatic heart disease

52
Q
• 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
A

Infective endocarditis

53
Q

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

A

Infective endocarditis

54
Q

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

A

Infective endocarditis

55
Q
• 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

A

Congenital Heart Disease

56
Q
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
A

Congenital heart disease

57
Q

• Malformations causing
Right-to-Left Shunts:
_________

A

Cyanosis

58
Q

• Malformations causing
Left-to-Right Shunts:
________

A

– Most common

59
Q
\_\_\_\_\_\_\_ 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
A

Right to left shunts

60
Q
• 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
A

Tetralogy of fallot

61
Q
\_\_\_\_\_\_\_\_ 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
A

Left-to-Right Shunts

62
Q
• 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)
A

Patent Ductus Arteriosus: Connects Pulmonary Artery and Aorta

63
Q
• Obstructive defect located in the 
area of the ductus that may be 
asymptomatic until adulthood
• Rib notching due to collateral 
circulation
• Males 2:1
A

Coarctation of the Aorta

64
Q

Is there hypo or hypertension proximal to coarction?

A

Hypertension

65
Q

Is there hypo or hypertension distal to coarction?

A

Hypotension