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Spp Amp > Cvs: Atherosclerosis > Flashcards

Cvs: Atherosclerosis Flashcards

1
Q

Atherosclerosis is characterized by lesions called __________ or ______________ plaques

A

atheromas or atheromatous/fibrofatty

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2
Q

Atherosclerosis ___ & _____ vascular lumen weakening the underlying media

A

protrude into and obstruct

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3
Q

3 morphologic patterns of arteriosclerosis are

A

ATHEROSCLEROSIS

Monckeberg Medial Calcific Sclerosis

Arteriolosclerosis

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4
Q

AMERICAN HEART ASSOCIATION CLASSIFICATION OF ATHEROSCLEROSIS

Type 1
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type I (initial) lesion
Isolated macrophages
By lipid accumulation
From first decade
Clinically silent

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5
Q

Type II
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type II (fatty streak) lesion
Intracellular lipid accumulation
By lipid accumulation
From first decade
Clinically silent

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6
Q

Type III
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type III (intermediate)
Type II changes + small extracellular lipid pool
By lipid accumulation
From third decade
Clinically silent

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7
Q

Type IV
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type IV (atheroma)
Type II changes + core of extracellular lipid
By lipid accumulation
From third decade
Clinically silent or overt

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8
Q

Type 5
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type V (fibroatheroma)

Lipid core and fibrotic layer, multiple or calcific or fibrotic mainly

Accelerated smooth muscle and collagen increase

From fourth decade

Clinically silent or overt

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9
Q

AMERICAN HEART ASSOCIATION CLASSIFICATION OF ATHEROSCLEROSIS

Type VI
NOMENCLATURE
HISTOLOGY
GROWTH
ONSET
CLINICAL MECHANISM CORRELATION

A

Type VI (complicated)
Surface defect, hematoma- haemorrhage, thrombus
Thrombus, hematoma
From fourth decade
Clinically silent or over

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10
Q

the cause of atheroma is ____& ______

A

complex and multifactorial

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11
Q

There are many risk factors. The various risk factors are considered in _____ main groups by some authors.

Name the groups

A

3

A) ENDOGENOUS FACTORS
B) ENVIRONMENTAL FACTORS
C) DISEASES

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12
Q

A) Endogenous factors include:

A

1 Age
2 Sex
3 Genetic factors
4 Racial differences

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13
Q

Endogenous factor:
1. Age
• atherosclerosis is a slow complex disease that typically starts in______ and often progresses when people grow older.
• In some people it progresses rapidly even in the ________ decades.

A

childhood

third

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14
Q

Endogenous factor:
2. Sex
• in men risk increases after the age of__ and in woman risk increases after the age __.

A

45
55

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15
Q

• The lower incidence of ischemic heart disease in women, especially in premenopausal age, is probably due to high levels of ________ & _________, both of which have anti- atherogenic influence.

A

oestrogen and high- density lipoproteins

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16
Q

• ENDOGENOUS FACTORS:
3. Genetic factors
• A well-established familial predisposition to atherosclerosis and ischaemic heart disease is most likely ______.

A

polygenic

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17
Q

Genetic defects in lipoprotein metabolism causing _________________ are associated with accelerated atherosclerosis,

• e.g homozygous familial hypercholesterolemia which often results in ____________ before age 20 years

A

hyperlipoproteinemia

myocardial infarction

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18
Q

Geneticfactors
• It is caused by the defects in the LDL leading to inadequate _______ uptake of LDL and markedly increasing circulating LDL.

There is family history of ischaemic heart disease in ___________ & _______

A

hepatic

diabetes mellitus and hypertension.

19
Q

ENDOGENOUS FACTORS:
4. Racial differences

• there is a striking difference in obesity between white and black women,

• higher fasting blood glucose and greater prevalence of diabetes in blacks and lower ____ values than in white men.

A

HDL

20
Q

B) Environmental factors

1• _________ incidence of atherosclerosis in developed countries and ______ prevalence in underdeveloped countries, suggests the role of environmental influences.

A

Higher

Low

21
Q

of all the known risk factor, __________ seems to be the most important determinant of the geographic differences in the incidence of atherosclerotic coronary artery disease.

A

serum cholesterol

22
Q

ENVIRONMENTAL FACTORS
2. Cigarette smoking
There is substantial greater mortality from cigarette smoking.
• The death rate depends on number of cigarettes smoked.
• Cigarette smoking alter lipid profile. Low levels of _____ and higher values of _______ and _________ have been documented in heavy smokers

A

HDL

LDL and triglycerides

23
Q

Mechanism involved in cigarette smoking

Endothelial injury consequent to ____________ and ___________ that results in rapid aggregation of platelets in smokers

A

carbon monoxide exposure
chronic hypoxia

24
Q

Cigarette smoking is a major risk factor for developing coronary artery disease, producing a marked decline in______________.
It causes endothelial dysfunction, possibly through increased _________, and this is also true for passive smoking or environmental tobacco smoke.

A

endothelium dependent vasomotor response

oxidative stress

25
Q

. Significant increases in _____ &_______are demonstrable in smokers and __________metabolites are reduced significantly.

A

sICAM-1 and sVCAM-1

nitric oxide

Soluble Intercellular adhesion molecule 1 (ICAM-1) and soluble vascular cell adhesion molecule 1 (VCAM-1)

26
Q

ENVIRONMENTAL FACTORS
3. Hyperlipoproteinemia and diet
If saturated fats are abundant in the diet, the concentration of ______ in the plasma tend to be high.
Diet rich in saturated fats and cholesterol is_____. Unsaturated fat is not. Excessive refined carbohydrates sucrose increases blood_________.

A

LDL

androgenic

blood lipid cholesterol lipoprotein.

27
Q

ENVIRONMENTAL FACTORS
4. Lack of exercise
• physical activity may reduce the incidence of complicated ________. It has been shown that people with sedentary life style generally suffer more from coronary artery disease than those with strenuous jobs.

A

Atheroma

28
Q

Individual with coronary prone behaviours such as time urgency, aggressiveness, ambition, competitiveness _______ personality) have a_________ increase risk of coronary artery disease compared with _______ behaviour of relaxed and happy- go-lucky type

A

Type A

two- to three-fold

type B

29
Q

ENVIRONMENTAL FACTORS
5. Atherosclerosis is more common in ____ socioeconomic person.

A

Low

30
Q

• ENVIRONMENTAL FACTORS
6. Alcohol
• A moderate intake of alcohol (____units a day) appears to offer some protection from coronary disease; however heavy drinking is associated with _________&__________

A

2 to 4

hypertension and excess cardiac events

31
Q

Factor C?

A

Diseases

(High blood pressure.
High cholesterol.
High triglycerides, a type of fat (lipid) in the blood.
Diabetes.
Insulin resistance.
Obesity.
Inflammation from an unknown cause or from diseases such as arthritis, lupus, psoriasis or inflammatory bowel disease)

32
Q

RISK FACTORS
• Can be classified in 3 different ways;

A

• Nonmodifiable vs Potentially Controllable
• Major vs lesser/uncertain
• Genetic vs non-genetic

33
Q

• Nonmodifiable vs Potentially Controllable

A

• Increasing Age
• Male gender
• Family history
• Genetic abnormalities

• hyperlipidaemia
• hypertension
• Cigarette smoking
• diabetes

34
Q

Major vs lesser/uncertain

A

• High Cholesterol and Triglyceride levels
• Hypertension
• Cigarette smoking
• Type I diabetes
• Physical inactivity
• High saturated fat
• Obesity

• alcohol
• Lipoprotein level
• hardened (trans)unsaturated fat intake
• Chlamydia pneumoniae

35
Q

Risk factor classification 3

A

Genetic vs non-genetic

36
Q

List the 8 theories of pathogenesis of atherosclerosis

A
  1. INSUDATION HYPOTHESIS/VIRCHOW’S IMBIBITION THEORY
  2. ENCRUSTATION THEORY
  3. THROMBOGENIC HYPOTHESIS
  4. REACTION TO INJURY HYPOTHESIS
  5. INTIMAL SMOOTH MUSCLE PROLIFERATION
  6. ROLE OF LOOD MONOCYTES
  7. ROLE OF HYPERLIPIDAEMIA
  8. MONOCLONAL HYPOTHESIS
37
Q

INSUDATION HYPOTHESIS/VIRCHOW’S IMBIBITION THEORY

• Virchow holds that atheromatous deposits are lined by vascular endothelium
• Hence ______ from plasma is imbibed through endothelium (by stress) where it splits into ________ and ______
• These are retained and deposited while PLs (phospholipids?)are removed in the circulation.
• There is sub-intimal connective tissue proliferation by FB??? reaction towards cholesterol

A

B Lipoprotein (Lp)

cholesterol and its esters

(According to this theory there is proliferation of intimal cells due to insudation of lipids and plasma proteins into the vessel wall. However how lipids enter the vessel wall is not clear)

38
Q

• ENCRUSTATION THEORY
• First suggested in the ____ century by______

A

19th

Rokitansky

39
Q

Rokitansky asserted that _______ is deposited on the inner surface of aas???? and leads to thickening of the inner lining
• A mordern version of this theory holds that______ represents the initial event in atherosclerosis
• Organization of these thrombi leads to the formation of plaques & expansion of these lesions reflects repeated episodes of thrombosis & organization

A

materials from blood

thrombi

40
Q

THROMBOGENIC HYPOTHESIS
• This proposes that thrombus is incorporated
into the _____ of blood vessels
• Lipid is derived from cell membrane and cells stimulated to proliferation by _______

A

intima

Platelet derived growth factors PDGFs

41
Q

Response to injury hypothesis

A

According to this hypothesis atherosclerosis is a chronic inflammatory and healing response of the arterial wall to the endothelial injury

Lesion progresses by interaction of modified lipoproteins, monocyte derived macrophages and T lymphocytes with endothelial cells and smooth muscle cells of the arterial wall

42
Q

Type 6 atherosclerosis classification is related to

A

Dystrophic calcification

{This happens after you’ve had plaque (fat and cholesterol) forming in your arteries (atherosclerosis) for about five years. Build up of calcium in your vessels }

43
Q

What is the fate of a plaque

A
  1. Fracture: Surface
    Emboli
  2. Dissolve
  3. Weakening of wall —> Aneurysm
  4. Calcification
  5. Ulceration

Spp Amp (3 decks)

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