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DMD 5247 > blood vessel pathology > Flashcards

blood vessel pathology Flashcards

1
Q

origins of atherosclerosis

A

d

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2
Q

What is the most common form of arteriosclerosis

A

atherosclerosis

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3
Q

what is atherosclerosis

A

a narrowing and hardening of arteries due to intimal atheromas (atherosclerotic plaque)

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4
Q

What are the vessels most affected by atherosclerosis

A 
abdominal aorta
coronary arteries
popliteal arteries
carotid arteries
vessels of the circle of willis
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5
Q

what are the contents of an artherosclerotic plaque

A

fibrous cap
lipid core
necrotic center (cell debris, cholesterol, foam cells, and calcium)

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6
Q

What are the steps of atherosclerosis development

A
  1. chronic endothelial injury
  2. endothelial dysfunction/monocyte adhesion and immigration
  3. macrophage activation/ smooth muscle recruitment
  4. leukocytes and smooth muscle engulf lipid
  5. smooth muscle proliferation/ collagen and extracellular lipid deposition
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7
Q

what can cause chronic endothelial injury

A 
hypertension
hyperlipidemia
smoking
toxins
viruses
immune reactions
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8
Q

what happens when high blood pressure damages the endothelium of blood vessels

A

it causes inflammation. mostly in areas of turbulent flow, this increases cholesterol invasion/plaque formation

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9
Q

What are the risk factors for atherosclerosis

A 
age
gender
genetics
lifestyle*
smoking 
diabetes
inflammation
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10
Q

What are the complications caused by atherosclerosis

A

stenosis
thrombus/embolism
aneurism
calcification

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11
Q

how does LDL increase atherosclerosis

A

OXIDIZED LDL causes adhesion and entry of monocytes, then the monocytes turn into macrophages, which consume the LDL and turn into a foam cell. foam cells release growth factors that encourage atherosclerosis

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12
Q

what are the two types of LDL

A

type A = large less dense

type B = small more dense

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13
Q

which is the worse type of LDL, type A or type B

A

type B. it is smaller so it can fit through the endothelium more easily, and it is more dense so it bounces along the endothelium more, causing it again to be more likely to penetrate the endothelium

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14
Q

what determines which type of LDL you have more of

A

genetics, oral contraceptives, and diet

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15
Q

what kind of diet increases type B LDL

A

low fat, high carb diets

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16
Q

is LDL type B commonly measured in a blood test? if not, what is a good substitute?

A

it can be measured but usually isn’t

TG:HDL is a good surrogate

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17
Q

what is a good TG:HDL level

A

less than 1.5 is good, less than 2 is recommended

18
Q

what diet decreases both LDL type B and TG:HDL levels

A

a low carb, high fat diet

19
Q

what must occur for cholesterol to be a problem in atherosclerosis

A

is must be oxidized.

20
Q

how do we prevent our LDL from being oxidized and becoming problematic

A

antioxidant therapy
exercise
keto diet

21
Q

what does the HMG CoA reducatase enzyme do

A

it causes cholesterol to be synthesized

22
Q

what actiavates, and what deactivates HMG CoA reductase

A

insulin activates, glucagon inactivates

23
Q

what drugs inhibit HMG CoA reductase

A

statins

24
Q

What are the negative side effects of statins

A 
increase risk of diabetes
kidney failure
liver failure
muscle pain (myopathy )
reduces ubiquinone
reduced important cholesterols
25
Q

What are the potential problems caused by statins reducing ubiquinone (electron carrier in the ETC of the mitochondria)

A

muscle break down (rhabdomyelosis)
muscle weakness and pain
reduced mitochondrial function (oxidative stress)
cataracts

26
Q

what is the most cost effective treatment of coronary heart disease

A

aspirin

27
Q

what are the 5 cholesterol containing things that are important that can be reduced by statins

A 
cell membrane cholesterols
steroid synthesis
ubiquinone
bile salts
vitamin D
28
Q

what are the two types of hypertension

A

benign and malignant

29
Q

what are the two types of benign hyper tension

A

essential or primary and secondary

30
Q

what is essential or primary hypertension

A

idopathic hypertension that arises from a mix of genetic and environmental factors

31
Q

what is seconday hypertension

A

hypertension resulting from

structural renal, or endocrine defects

32
Q

what are the symptoms of malignant hypertension

A 
>200/120 mm/hg
lethal in 1-2 years if untreated
renal failure
retinal hemorrhages
papilledema
33
Q

what is the major pathogenic defect that initiates the hypertensive process

A

insulin resistance

34
Q

what are the 5 ways insulin resistance affects hypertension

A

RAAS dysfunction (antidiuretic, increased bp)
enhanced growth factor (thicker vessel walls)
SNS activity increase (increased heart rate)
dyslipidemia (less HDL, more LDL type B)
decrease in Nitric oxide (NO is vasodilator)

35
Q

what is an aneurism

A

local abnormal vessel dilation

36
Q

what is an aneurism

A

local abnormal vessel dilation

37
Q

what causes aneurisms

A 
atherosclerosis
wall degeneration
trauma
conginital defects (marfan)
infection
38
Q

what is aortic dissection

A

aneurism of the aorta

39
Q

what are the types of aortic dissection

A 
1 = both ascending and descending
2 = ascending only
3 = descending
40
Q

what are the four types of vessel tumors

A

hemangioma - common and benign
glomus tumor - benign but painful
kaposi sarcoma - low malignant
angiosarcoma - highly malignant

DMD 5247 (11 decks)

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