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DMD2 sem 2 > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

important

A

Be familiar with arteries, vessels, and lymphatic system and things that could go wrong

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2
Q

What is the best way to distinguish between an artery and a vein?

A

Wall thickness is the best way to differentiate veins and arteries

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3
Q

What structures are found in all blood vessel types?

A

Endothelial cells

Smooth muscle cells

Extracellular matrix

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4
Q

What can happen if there are changes in wall thickness?

A

Changes in wall thickness can lead to atherosclerosis and hypertension

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5
Q

What are the layers of the blood vessels?

A

Tunica intima (inside)

Tunica media (Most closely packed fibers)

Tunica adventitia (most external)

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6
Q

What are the components of

A

Intima consists of a single layer of endothelial cells

Basement membrane

thin layer of extracellular matrix

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7
Q

What does relative size of tunica media and adventitia tell us?

A

If media is bigger than adventitia there is lots of muscle therefore it is an artery. Vice versa for vein

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8
Q

What can go wrong with blood vessels?

A

Blockage (preceded by narrowing)

Rupture (Preceded by weakening)

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9
Q

What does turbulent blood flow result in?

A

Turbulent blood flow can result in inside of blood vessel activating the coagulation cascade (can be because of an injury)

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10
Q

What happens in response to vascular wall injury?

A

Adhesion molecules become activated (endothelial activation) and attach to the platelets

Cytokines are released to attract repair

Vasoactive compounds are released (constriction factors mostly but some dilation to create a balance to prevent blood from shutting off completely)

Smooth mulscles develop, grow and remodel

Intimal thickening takes place

Increased expression of procoagulants, and proinflammatory markers.

Altered expression of chemokines, cytokines, and growth factors.

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11
Q

What factors can induce vascular wall injury?

A

Turbulent flow

Hypertension

Cytokines

COmplement

Bacterial products

Lipid products

Advanced glycation end products

Hypoxia, acidosis

Viruses

Cigarette smoke

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12
Q

What types of vascular pathology are there?

A

Vascular patholgoy is either blockage or rupture

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13
Q

How does vascular wall thickening?

A

Endothelium

Recruitment of smooth muscle cells or smooth muscle precursor cells to the intima

Smooth muscle cell mitosis

Elaboration of extracellular matrix

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14
Q

What are the blood pressure categories?

A 
Normal: <120; <80
Elevated: 120 - 129; <80
High blood pressure stage 1: 130 - 139; 80 - 89
HBP stage 2: 140 or higher; 90 or higher
Hypertensive crisis: >180;>120
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15
Q

What is blood pressure?

A

CO x TPR

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16
Q

What is CO?

A

Blood volume (Sodium, mineralocorticoids, ANP)

HR and contractility

17
Q

What factors affect TPR?

A

Humoral factors: Contrictors and dilators

Neural factors: alpha and beta adrenergic

Local factors: Autoregulation, pH, and hypoxia

18
Q

What does MI do to heart contractility?

A

MI leads to reduced contractility of the heart muscles it affects.

19
Q

What is renin and what does it do?

A

Renin is produced by the kidneys.

Renin converts ANGogen to ANG1 which is converted to ANG2 and increases vascular smooth muscle tone.

ACE inhibitors increase BP

20
Q

How many people are hypertensive?

A

~29% of people were hypertensive

21
Q

Which demographic has lower threshold for hypertension?

A

Threshold is lower in diabetic patients. Hypertension consequences are exacerbated by diabetes

22
Q

What causes hypertensive vascular disease?

A

Idiopathic or primary 90 - 95%

Secondary 5 - 10%

23
Q

What does hypertensive vascular disease result in?

A

Increased risk of atherosclerosis

Cardiac hypertrophy

Heart failure

Aortic dissection

Multi-infarct dimentia

Renal failure

24
Q

What demographic has the most severe and prevalent incidence of hypertensive vascular disease?

A

African-Americans

25
Q

What happens if hypertension is undiagnosed?

A

If left untreated, 50%of patients may die of ischaemic heart disease

5% of patients die of rapidly rising blood pressure

26
Q

What percentage of strokes, heart disease, and all cause mortality is due to undiagnosed hypertension?

A

62% of strokes

49% of ischaemic heart disease cases

13% of all-cause mortality worldwide

27
Q

What is the outcome of reduction of diastolic BP?

A

Lowering diastolic BP by 5mmHg results in 34% reduction in stroke risk

28
Q

What is arteriolosclerosis?

A

Hardening of the arteries. (Artery wall thickening and loss of elasticity)

29
Q

What are the patterns of arteriolosclerosis?

A

Patterns:

Arteriolosclerosis

Small arteries and arterioles

May cause downstream ischemic injury

Monckeberg medial sclerosis

Calcification of the wall of arteries

Atherosclerosis

The most important

30
Q

What is the outcome of atherosclerotic plaques in the blood vessels?

A

If stable: Blood moving fast results in slowing down at the Thickening leading to potential clotting of the blood vessel.

If unstable: Ruptures and fat can enter blood stream and cause emboli to form.

31
Q

What determines likelihood of atherosclerosis?

A

Likelihood determined by:

Acquired (cholesterol, smoking, HTN)

Inherited (LDL, receptor gene mutations)

32
Q

What are the risk factors for atherosclerosis?

A

Genetic: rarely mendelian, often polygenic (familial inflammatory conditions)

Age: 40 - 60

Gender: Males and females post menopause

33
Q

What causes cardiomegaly?

A

Hypertrophy (increased weight or thickness)

Dilation (chamber size larger)

34
Q

What causes cardiomegaly?

A

Could be due to compensatory changes as a result of:

Heart disease

Volume/pressure overload

35
Q

What is the contractile unit called in the heart?

A

Myocytes: Contraction unit is called a sarcomere

36
Q

What is the most common form of arrhytmia?

A

Atrial fibrillation

37
Q

What is a potential outcome of atrial fibrillation?

A

It can lead to a blood clot to form which can become a thromboembolism

38
Q

What are the important coronary arteries to know?

A

Left and right

Left: LAD and LCX

Right

39
Q

What kind of metabolism do cardiomyocytes need and what happens if there is an infarction?

A

Energy from oxidative phosphorylation and if no oxygen they can die from hypoxia

DMD2 sem 2 (97 decks)

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