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Pathology > Cardiovascular Pathology: Overview > Flashcards

Cardiovascular Pathology: Overview Flashcards

1
Q

Atherosclerosis is

A

a Pathological change in the wall of the artery.

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2
Q

Number 1 cause of death in Canada is:

A

Atherosclerosis, responsible for MI, stroke, aneurysm, peripheral vascular disease)

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3
Q

Tunica intima:

A

layer of endothelial cells

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4
Q

Tunica media:

A

smooth muscle

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5
Q

Tunica externa:

A

connective tissues

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6
Q

Fatty streak is:

A

universal lipid accumulation in proliferating intima. Occur almost to everyone over 20.

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7
Q

Fibrous tissue accumulate in the intima is called

A

atherosclerosis (Abnormal)

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8
Q

Major clinical Manifestations of Atherosclerosis:

A
  • Usually asymptomatique
  • Angina
  • MI
  • Transient Ischemic Attack
  • Ischemic stroke
  • Peripheral Arterial Disease
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9
Q

Angina vs MI:

A

Angina: partially occluded the coronary artery, when there is activity, increase demand in supply but cannot meet the demand on O2.
MI: Completely occluded, pain is more severe.

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10
Q

Transient Ischemic Attack vs Ischemic stroke:

A

TIA: partially occluded the vessel in the brain.

Ischemic stroke: completely occluded in the brain.

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11
Q

Peripheral Arterial Disease:

A

not enough blood flow to the legs causing intermittent claudication. During activity, blood flow to the legs become inadequate and they will experience pain. As it progress, pain can be experienced at rest.

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12
Q

Key components of the pathogenesis of Atherosclerosis:

A

Endothelial dysfunction

Chronic Inflammation

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13
Q

Damage to the endothelium due to:

A
  • Hyperlipidemia
  • Hypertension (physical injury)
  • Smoking (7000+ compounds, some damage the endothelium)
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14
Q

Damage to the endothelium cause the cell to become dysfunctional or altered:

A
  • Increase permeability
  • Platelets and lymphocytes release mediators (Platelets release PDGF and lymphocyte release IL-1 and IFN)
  • Monocytes release MDGF as they migrate into the tunica media vessel wall (do not belong there) and become macrophages
  • Fibroblasts and smooth muscles cells get involved and release other mediators (eg. growth factors)
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15
Q

Which region of the vessel, the endothelium is more vulnerable to hemodynamic stress (Hypertension)?

A

The branch point, at the bifurcation.

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16
Q

Which region of the vessel, the endothelium is more vulnerable to developing plaque?

A

The branch point, at the bifurcation.

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17
Q

Inflammatory component of atherosclerosis: involve T-cells and Macrophages

A
  • Monocytes migrate into the wall of the vessel, particles of LDL are able to access the inner wall, which damage the endothelium.
  • Inside the wall of the vessels, macrophages (have a specific receptor for LDL) swallow a lot of LDL and becomes a foam cell.
  • Release of cytokine and free radical
  • Necrosis in the middle of the plaque starts to form as these are accumulating and a fibrous cap is formed (create an extracellular matrix)
  • Inflammation in the vessel wall, the smooth muscle cells become involved and start proliferating in direction of the tunica intima due to signaling molecules. (mitosis)
  • Smooth muscles cells change properties (accumulate lipid, become foam cells, synthesize collagen, elastin and glycoprotein)
  • Lymphocytes get involve too, a fatty streak is developed and get bigger and bigger.
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18
Q

Lipoproteins role:

A

Allows the transportation of lipid in an aqueous medium (eg. blood)

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19
Q

Lipoprotein component:

A

Inside the lipoprotein (triglycerides and cholesterol)

On the surface (Apo proteins and phospholipids)

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20
Q

Accumulation of lipoprotein:

A
  • Protein on the surface are distrinctive (allow different cells to recognize the different lipoproteins and take them in)
  • Lipoprotein are absorbed in chylomicrons from interstine.
  • Chylomicron absorbs the fats and brings them to the liver.
  • The liver repackages them, altered them, lipoproteins get removed, until the end product: HDL
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21
Q

4 types of lipoproteins:

A

Very low-density lipoproteins (VLDL)
Intermediate density lipoproteins (IDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)

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22
Q

Distinction between the type of lipoproteins?

A

Higher density = Higher amount of protein

23
Q

HDL is referred to be a good ones because:

A

Transport lipids back to the liver. (remove the cholesterol from cells)

24
Q

LDL, VLDL and IDL are referred to be a bad one because:

A

Transport lipids throughout the circulation and are able to deposits them into the walls of the vasculature. (Release cholesterol)

25
Q

Lipoprotein lipase:

A

Breakdown the triglycerides and stores it in the fat cells. (Adipocytes)

26
Q

LDL contain a lot of:

A

Cholesterol

27
Q

VLDL contains:

A

triglycerides (3 fatty acids)

28
Q

On the surface of LDL there are:

A

APO-B proteins

29
Q

The LDL bind to the LDL receptors in our cells with the help of:

A

APO-B

30
Q

Lipoprotein entering into our cells:

A
  • With the help of APO-B
  • Internalized into an endosome
  • The structure separate into 2 parts: The part contain the receptor, is sent to the plasma membrane to be reclycled. The second part, a lysosome will free the LDL from the endosome.
  • The cholesterol will enter in the cytoplasm and can be used to build structures within the cell. (will take only the necessary amount to build the membrane/strucutre)
31
Q

Phenotypic modulation is

A

the contractile smooth muscle cells which becomes a foam cells due to mediators from macrophages and becomes a synthetic cell capable to making collagen and fibrous cap.

32
Q

Bone marrow role in the formation of atherosclerotic plaque:

A

Stem cells which can differentiate into smooth muscle progenitor cells which become part of the fibrous cap. (which also attempt to repair the endothelial injury)

33
Q

Risk Factors for atherosclerosis:

A
  • Hyperlipidemia
  • Hypertension
  • Smoking
  • Toxins
  • Hemodynamic factors
  • Immune reactions
  • Viruses
34
Q

Lifestyle Factors increasing the risk for cardiovascular disease:

A
  • Hyperlipidemia and hypertension related to alimentation
  • Smoking
  • Type II diabetes
  • Obesity
  • Sedentary
35
Q

Stable Plaques vs Unstable plaques:

A

The stable plaque has a thicker fibrous cap and a small, hard fatty core.
The unstable plaque has a thin fibrous cap and a large, soft fatty core. (more prone to rupture)

36
Q

If a plaque rupture, what happened?

A

It triggers the formation of a blood clot which can completely occlude the vessel.

37
Q

As atherosclerosis progresses, change in the elastic tissues in the wall of the vessel happen:

A

The vessel walls are affected and become weaker. (can lead to an aneurysm. The wall bulge out due to the pressure)

38
Q

A rare genetic defect in LDL receptors (familial hypercholesterolemia):

A

A Genetic abnormality in the structure of the LDL receptor, which as a consequence that LDL cannot bind or enter the cell, so stay in the circulation
Another genetic abnormality can be also found in APO-B.

39
Q

Drugs acting on the PCSK9 for tx hyperlipidemia action:

A

Drugs block the PCSK9 (PCSK9 normally destroy LDL receptor in the liver, so more LDL in the circulation) so more LDL Receptor, more LDL pull out from the circulation.

40
Q

The Triad of hyperlipidemia:

A
  • Elevated triglycerides (VLDL)
  • Small LDL particles
  • Low HDL
41
Q

T or F: Eating Eggs can have an effect on cholesterol, and be an additive risk factor for atherosclerosis:

A

False. Do not have that much cholesterol.

42
Q

Best oil:

A

Canola oil

43
Q

Saturated vs non-saturated Fats: which one is a risk factors to develop atherosclerosis?

A

Saturated Fats (tend to decrease LDL receptors, so more lipids and cholesterol in the circulation)

44
Q

Main cause of diabetes II:

A

Obesity

45
Q

Diabetes is:

A

when the Islets of Langerhans’s are not making enough insulin in type I diabetes or being resistant to the insulin.

46
Q

Metabolic Syndrome signs and symptoms:

A 
-Abdominal obesity
Hyperinsulinemia (but being resistant to it)
-High fasting plasma glucose
-Impaired glucose tolerance
-Hypertriglyceridemia
-Low HDL and high LDL
-Hypertension
47
Q

Insulin role:

A
  • increase the ability to intake amino acids and glucose into the cell.
  • Glucose in the cells is used to make proteins.
  • Free fatty acids in the cells are used to make triglycerides.
  • Insulin allows us to insert the glucose transporter into the cell membrane to move glucose into the cells.
48
Q

What happen with the free fatty acids if you are diabetes?

A

The free fatty acids are not being taken in because the insulin receptor is not working as well. There are more LDL floating around, that are ready to be taken into foam cells.

49
Q

Microvascular disease related to diabetes:

A
  • Capillary vasoconstriction
  • Permeability increase
  • Abnormal extracellular matrix
  • Edema, ischemia, neovascularization
  • Cause problems in the periphery and in the eye.
50
Q

Artherosclerosis related to diabetes:

A
  • Endothelial damage due to insulin resistance and hyperglycemia
  • Glucose-derivatives react with intracellular and extracellular proteins, damage the extracellular matrix
  • May involve superoxide production by mitochondria.
51
Q

Diabetes cause Inflammation can be measured by:

A

C-reactive protein

52
Q

The risk of diabetes is directly related to:

A

Weight change since age 21.

53
Q

The Triad of venous thrombosis:

A
  1. Poor blood circulation
  2. Venous injury
  3. Increased blood clotting

Pathology (23 decks)

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