Atherosclerosis 2 Flashcards

1
Q

Which of the following statements are true?
Arteriosclerosis is a general term describing any hardening of medium or large arteries
Arteriosclerosis is a general term describing any hardening of small arteries
Atherosclerosis is a hardening of an artery specifically due to an atheromatosus plaque formation
Arteriolosclerosis is a hardening of medium arteries

A

Arteriosclerosis is a general term describing any hardening of medium or large arteries

Atherosclerosis is a hardening of an artery specifically due to an atheromatosus plaque formation

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2
Q

Which of the following statements are NOT true?
Arteriosclerosis is a general term describing any hardening of medium or large arteries
Arteriosclerosis is a general term describing any hardening of small arteries
Atherosclerosis is a hardening of an artery specifically due to an atheromatosus plaque formation
Arteriolosclerosis is a hardening of medium arteries

A

Arteriosclerosis is a general term describing any hardening of small arteries

Arteriolosclerosis is a hardening of medium arteries

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3
Q

Which of the following statements are true?
Arteriolosclerosis is a general term describing any hardening of small arteries
Arteriosclerosis is a general term describing any hardening of medium or large arteries
Atherosclerosis is a hardening of an artery specifically due to an atheromatosus plaque formation
Arteriosclerosis is a hardening of small arteries

A

Arteriolosclerosis is a general term describing any hardening of small arteries
Arteriosclerosis is a general term describing any hardening of medium or large arteries
Atherosclerosis is a hardening of an artery specifically due to an atheromatosus plaque formation

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4
Q
 The clinical manifestations of atherosclerosis:
 stroke
 dissection of the aorta
 arteriosclerosis obliterans
 diabetes mellitus
A

stroke

dissection of the aorta

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5
Q
 The clinical manifestation of atherosclerosis:
 Addison-kór
 myocardial infaction
 Waterhouse-Friderichsen syndrome
 acute mesenteric ischemia
A

myocardial infaction

acute mesenteric ischemia

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6
Q
 Non-modifiable risk factors of atherosclerosis:
 age
 gender
 family history
 Caucasian race
A

age
gender
family history

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7
Q
 Non-modifiable risk factors of atherosclerosis:
 hypertension
 female gender
 diabetes mellitus
    family history
A

female gender

family history
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8
Q
 Non-modifiable risk factors of atherosclerosis:
 dyslipidemia
 hypertension
 obesity
 age
A

age

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9
Q
 Modifiable risk factors of atherosclerosis:
 dyslipidemia
 hypertension
 obesity
 age
A

dyslipidemia
hypertension
obesity

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10
Q
 Modifiable risk factors of atherosclerosis:
 smoking
 heavy alcohol drinking
 sedentary lifestyle
 diabetes mellitus
A

smoking
heavy alcohol drinking
sedentary lifestyle
diabetes mellitus

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11
Q
 Modifiable risk factors of atherosclerosis:
 dyslipidemia
 obesity
 hypertension
 low income
A

dyslipidemia
obesity
hypertension

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12
Q
 Modifiable risk factors of atherosclerosis:
 Chlamydia pneumoniae infection
 Herpes virus infection
 CMV infection
 Hepatitis B infection
A

Chlamydia pneumoniae infection
Herpes virus infection
CMV infection

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13
Q
 Dyslipidemia which promotes atherosclerosis:
 VLDL↑
 LDL↑
 HDL ↓
 IDL↑
A

LDL↑

HDL ↓

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14
Q
 Characteristic features of atherogenic dyslipidemia:
 elevated serum TG level
 presence of small LDL in the serum
 decreased serum level of HDL
 Dysfibrinogenemia
A

elevated serum TG level

presence of small LDL in the serum

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15
Q
 Modifiable risk factors of atherosclerosis:
 elevated serum homocysteine
 elevated serum glucose
 psychosocial stress
 higher education
A

elevated serum glucose

psychosocial stress

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16
Q
 Components of the atherosclerotic plaque:
 smooth muscle cells
 macrophages
 lymphocytes
 cholesterol crystals
A

smooth muscle cells
macrophages
lymphocytes
cholesterol crystals

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17
Q
 Components of the atherosclerotic plaque:
 calcium 
 dendritic cells
 foam cells
 eosinophilic granulocytes
A

calcium

foam cells

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18
Q
 Components of the atherosclerotic plaque:
 smooth muscle cells
 macrophages
 lymphocytes
 eosinophilic granulocytes
A

smooth muscle cells
macrophages
lymphocytes

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19
Q
 NOT components of atherosclerotic plaque:
 calcium 
 dendritic cells
 foam cells
 eosinophilic granulocytes
A

dendritic cells

eosinophilic granulocytes

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20
Q

Which of the following factors contribute to the development of atherosclerosis according to lipid theory?
Infiltration of LDL into the arterial wall
The change of the TXA2/PGI2 ratio
The uptake of modified LDL by macrophages
Micro-injuries of the vascular intima promote platelet adhesion and aggregation

A

Infiltration of LDL into the arterial wall

The uptake of modified LDL by macrophages

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21
Q

Evidences supporting the lipid or infiltration theory:
cholesterol is found in the atherosclerotic vessel wall
epidemiologic observations
evidences of animal experiments
intervention studies

A

cholesterol is found in the atherosclerotic vessel wall
epidemiologic observations
evidences of animal experiments
intervention studies

22
Q

Which of the following factors contribute to the development of atherosclerosis according to thrombogenic theory?
Changes of the TXA2/PGI2 ratio
Infiltration of LDL into the arterial wall
Micro-injuries of the vascular intima promote platelet adhesion and aggregation
The uptake of modified LDL by macrophages

A

Changes of the TXA2/PGI2 ratio

Micro-injuries of the vascular intima promote platelet adhesion and aggregation

23
Q

Which of the following factors contribute to the development of atherosclerosis according to thrombogenic theory?
Hyaluronic acid content of intracellular matrix decreases
Changes of the TXA2/PGI2 ratio
Changes of the composition of extracellular matrix in vascular intima and media
Micro-injuries of the vascular intima promote platelet adhesion and aggregation

A

Hyaluronic acid content of intracellular matrix decreases

Changes of the composition of extracellular matrix in vascular intima and media

24
Q

Which of the following factors contribute to the development of atherosclerosis according to mesenchymal theory?
Micro-injuries of the vascular intima promote platelet adhesion and aggregation
Collagen fiber content is increased, while elastic fiber content is decreased in the intima and in the media
The uptake of modified LDL by macrophages
Decrease of the heparin/heparane sulphate content of vessels

A

Collagen fiber content is increased, while elastic fiber content is decreased in the intima and in the media

Decrease of the heparin/heparane sulphate content of vessels

25
Q

Based on the mesenchymal theory, what will induce the changes of extracellular matrix component in the vessels?
Stress → spasm of vasa vasorum → hypoxia
Smoking - nicotine → potentiates catecholamine effect → spasm of vasa vasorum → hypoxia
Hypertension → mechanical compression of vascular wall
Hyperlipidemia → spasm of vasa vasorum → hypoxia

A

Smoking - nicotine → potentiates catecholamine effect → spasm of vasa vasorum → hypoxia
Hypertension → mechanical compression of vascular wall

26
Q

Based on the mesenchymal theory, what will induce the changes of extracellular matrix component in the vessels?
Caffeine → dilation of vasa vasorum → increased collagen synthesis
Smoking - nicotine → decreased NO production → hypoxia
Hyperlipidemia → spasm of vasa vasorum → hypoxia
Hypertension → mechanical compression of vascular wall

A

Hypertension → mechanical compression of vascular wall

27
Q

Based on the mesenchymal theory, what will induce the changes of extracellular matrix component in the vessels?
Catecholamine → spasm of vasa vasorum → hypoxia
Smoking - nicotine → decreased NO production → hypoxia
Hypertension → mechanical compression of vascular wall
Hyperlipidemia → spasm of vasa vasorum → hypoxia

A

Catecholamine → spasm of vasa vasorum → hypoxia

Hypertension → mechanical compression of vascular wall

28
Q

Based on the mesenchymal theory, what will induce the changes of extracellular matrix component in the vessels?
Catecholamine → spasm of vasa vasorum → hypoxia
Caffeine → dilation of vasa vasorum → increased collagen synthesis
Smoking - nicotine → potentiates catecholamine effect → spasm of vasa vasorum → hypoxia
Hypertension → increased elasticity of vascular wall

A

Catecholamine → spasm of vasa vasorum → hypoxia

Smoking - nicotine → potentiates catecholamine effect → spasm of vasa vasorum → hypoxia

29
Q

Which of the following factors contribute to the development of atherosclerosis according to the aging theory:
The component of connective tissue of vessels and other tissues change by aging
The endothelial endothelin production is decreased by aging
The endothelial NO production is decreased by aging
Micro-injuries on vascular intima promote platelet adhesion and aggregation

A

The component of connective tissue of vessels and other tissues change by aging

30
Q

Which of the following factors contribute to the development of atherosclerosis according to the aging theory:
The endothelial endothelin production is increased by aging
The component of connective tissue of vessels and other tissues change by aging
The endothelial NO production is decreased by aging
The uptake of modified LDL by macrophages

A

The component of connective tissue of vessels and other tissues change by aging

31
Q

Which of the following factors contribute to the development of atherosclerosis according to the aging theory?
The uptake of modified LDL by macrophages
The component of connective tissue of vessels and other tissues change by aging
Micro-injuries on vascular intima promote platelet adhesion and aggregation
The changed composition of EC matrix potentiates platelets adhesion and aggregation

A

The component of connective tissue of vessels and other tissues change by aging

32
Q
 Which of the following pathogens play an important role in the development of atherosclerosis according to the inflammation theory?
 Cytomegalovirus (CMV)
 Herpes simplex virus (HSV1, HSV2)
 Chlamydia pneumoniae
 HBV
A

Cytomegalovirus (CMV)
Herpes simplex virus (HSV1, HSV2)
Chlamydia pneumoniae

33
Q
 Which of the following pathogens play an important role in the development of atherosclerosis according to the inflammation theory?
 Helicobacter pylori
 HCV
 Chlamydia pneumoniae
 HBV
A

Helicobacter pylori

Chlamydia pneumoniae

34
Q
 Which of the following pathogens do NOT play a role in the development of atherosclerosis according to the inflammation theory?
 Cytomegalovirus (CMV)
 Herpes simplex virus (HSV1, HSV2)
 Chlamydia pneumoniae
 HBV
A

HBV

35
Q
 Which of the following pathogens do NOT play a role in the development of atherosclerosis according to the inflammation theory?
 Helicobacter pylori
 HCV
 Chlamydia pneumoniae
 HBV
A

HCV

HBV

36
Q

Which of the following factors contribute to the development of atherosclerosis according to the response to injury hypothesis:
Endothelial injury induces platelet activation
Mediators released from activated platelets induce smooth muscle cell migration from the media into the intima
Composition of EC matrix is changed due to chronic inflammation
The changed EC matrix causes lipid deposition

A

Mediators released from activated platelets induce smooth muscle cell migration from the media into the intima
Composition of EC matrix is changed due to chronic inflammation

37
Q

Evidences supporting the response to injury hypothesis:
Atherosclerotic plaques contain cholesterol crystals
Distribution of the atherosclerotic plaques
The uptake of modified LDL by macrophages
Decreased endothelial production of NO/PGI2

A

Atherosclerotic plaques contain cholesterol crystals

Decreased endothelial production of NO/PGI2

38
Q

Evidences supporting the response to injury hypothesis:
Plaques develop in areas with increased shear stress
Atherosclerotic plaques contain cholesterol crystals
The risk to develop atherosclerosis is higher in those diseases which cause endothelial dysfunction
Atherosclerotic plaques contain lymphocytes

A

Atherosclerotic plaques contain cholesterol crystals
The risk to develop atherosclerosis is higher in those diseases which cause endothelial dysfunction
Atherosclerotic plaques contain lymphocytes

39
Q

The possible causes of the endothelial dysfunction based on the response to injury hypothesis:
Modified LDL (ox-LDL, small-LDL)
Pathogenic microorganisms (CMV, Chlamydia pneumoniae, etc)
Genetic alterations
Increased serum HDL concentration

A

Modified LDL (ox-LDL, small-LDL)
Pathogenic microorganisms (CMV, Chlamydia pneumoniae, etc)
Genetic alterations

40
Q

The possible causes of the endothelial dysfunction based on the response to injury hypothesis:
Mechanical injuries
Micro-injuries on vascular intima promote platelet adhesion and aggregation
Increased serum homocystein concentration
Increased serum VLDL concentration

A

Mechanical injuries

Increased serum homocystein concentration

41
Q

True statements about the unifying hypothesis:
The hypothesis unifies the lipid and the response to injury theories
The essence of this hypothesis is: the thrombogenic- and mesenchymal theories have common components
Modified LDL can also cause endothelial dysfunction
Smooth muscle cells in the plaque have clonal origin

A

The hypothesis unifies the lipid and the response to injury theories

42
Q

The atherogenic effect of homocysteine:
Homocysteine inhibits binding of tPA and decreases fibrinolysis
Homocysteine stimulates the proliferation of smooth muscle cells
It inhibits endothelial functions
Homocysteine increases thrombomodulin expression and activity, therefore increases the activation of protein C

A

Homocysteine inhibits binding of tPA and decreases fibrinolysis
Homocysteine stimulates the proliferation of smooth muscle cells
It inhibits endothelial functions

43
Q

The atherogenic effect of homocysteine:
it damages the endothelium
it decreases collagen synthesis in vessels
it is prothrombotic
it inhibits the proliferation of smooth muscle cells

A

it damages the endothelium

it is prothrombotic

44
Q

The atherogenic effect of homocysteine:
it inhibits platelet aggregation
it increases collagen synthesis in vessels
it inhibits the migration and the proliferation of smooth muscle cells
it increases the amount of ox-LDL by lipid peroxidation

A

it increases collagen synthesis in vessels

it increases the amount of ox-LDL by lipid peroxidation

45
Q

The role of ox-LDL in the development of atherosclerosis:
it decreases the endothelial PGI2/NO synthesis
it stimulates the migration and the proliferation of smooth muscle cells
it has chemotactic effect
it increases the proliferation of macrophages

A

it decreases the endothelial PGI2/NO synthesis

I personally think it has chemotactic effect too…?

46
Q

True statements about the metabolic syndrome:
It is not a disease, but rather a cluster of disorders of your body’s metabolism
the pear type obesity has higher risk
concomitance of certain risk factors dramatically increases the risk for ischemic heart diseases
Se LDL concentration is essential to diagnose metabolic syndrome

A

It is not a disease, but rather a cluster of disorders of your body’s metabolism

Se LDL concentration is essential to diagnose metabolic syndrome

47
Q
 Waist circumference for clinical diagnosis of metabolic syndrome:
 in men:  102 cm
 in women: 80 cm
 in women: 88 cm
 in men: 105 cm
A

in men: 102 cm

in women: 88 cm

48
Q
 Essential parameters to diagnose metabolic syndrome:
 Se HDL: > 1.4 mM
 visceral obesity
 Se LDL: > 2.4 mM
 Se TG: > 1.7 mM
A

visceral obesity

Se TG: > 1.7 mM

49
Q

Essential diagnostic criteria of metabolic syndrome:
fasting blood glucose: > 5.6 mM
waist circumference in men > 102 cm; in woman: > 88 cm
Se HDL in men: < 1.0 mM; in woman: < 1.3 mM
Se TG: < 1.7 mM

A

fasting blood glucose: > 5.6 mM
waist circumference in men > 102 cm; in woman: > 88 cm
Se HDL in men: < 1.0 mM; in woman: < 1.3 mM

50
Q

Essential diagnostic criteria of metabolic syndrome:
RR: > 135/85 Hgmm
waist circumference in men: > 102 cm; in women: > 88 cm
Se HDL in men: < 1.0 mM; in women: < 1.3 mM
Se TG: < 1.7 mM

A

RR: > 135/85 Hgmm
waist circumference in men: > 102 cm; in women: > 88 cm
Se HDL in men: < 1.0 mM; in women: < 1.3 mM

51
Q
 Which factors increase the risk of developing metabolic syndrome?
 age
 smoking
 polycystic ovarium syndrome
 hyperthyroidism
A

age

polycystic ovarium syndrome