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DMD 5247 > Bikman - BV Path > Flashcards

Bikman - BV Path Flashcards

1
Q

What is atherosclerosis?

A
  • The most common form of arteriosclerosis.
  • A narrowing and hardening of arteries due to intimal atheromas
  • Atherosclerotic plaque
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2
Q

What vessels are most affected by atherosclerosis?

A
  1. Abdominal aorta
  2. Coronary arteries
  3. Popliteal arteries
  4. Carotid arteries
  5. Vessels of the circle of Willis
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3
Q

What are the contents of a plaque in atherosclerosis?

A
  1. Fibrous cap
  2. Lipid Core/Necrotic center
    - Cell debris, cholesterol or foam cells, Ca2+)
  3. Media
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4
Q

What factors can induce chronic endothelial “injury” that leads to atherosclerosis progression?

A
  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Toxins
  • Viruses
  • Immune reactions

Doesn’t have to be a tearing of the endothelium

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5
Q

What are the steps of atherosclerosis progression?

A
  1. Chronic endothelial “injury”
  2. Endothelial dysfunction. Monocyte adhesion and emigration.
  3. Macrophage activation. SM recruitment. Cytokines recruit other lymphocytes.
  4. Leukocytes and SM cells engulf lipid.
    * Hyperlipidemia is likely a primary player in etiology*
  5. SM proliferation. Collagen and EC lipid deposition (complicated plaque)
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6
Q

How are atherosclerosis and BP related?

A

High BP damaged the endothelium and activates inflammation.

  • Promotes turbulent flow in a BV
  • Turbulent flow is evident in areas of branching or constriction of the BV
  • Turbulent flow damages the endothelium
  • Endothelial damage increaseslikelihood of cholesterol invasion/clot formation
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7
Q

What are the two categories of major risk factors of atherosclerosis?

A

Non-modifiable

  • Age
  • Gender
  • Genetics

Modifiable

  • Lifestyle
  • Smoking
  • Diabetes
  • Inflammation
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8
Q

What are complications of atherosclerosis?

A
  1. Stenosis
  2. Thrombosis/embolus
  3. Aneurysm
  4. Calcification
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9
Q

What modification is necessary for cholesterol to be pathogenic?

A

Oxidation

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10
Q

Does cholesterol have any impact on heart disease or mortality?

A

Very little

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11
Q

Two LDL cholesterol patterns/types?

A

A type
- Large, less dense

B type
- Small, more dense

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12
Q

Which LDL cholesterol type penetrates endothelium more easily?

A

B type

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13
Q

What are risk factors for pattern B cholesterol?

A

Genetics
Oral contraceptives
Diet

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14
Q

What kind of diet can induce LDL type B expression?

A

Low fat, high carb

-Can therefore increase heart disease

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15
Q

How can we measure LDL-B cholesterol?

A

LDL-S3 GGE test to measure the diameter of the LDL

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16
Q

What is a good surrogate to measure LDL-B in the absence of LDL-B measurements? What should the ideal value be?

A

TG:HDL ratio (

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17
Q

Do low fat diets increase or decrease heart disease risk for some?

A

Increase; increased dietary fat improved every lipid blood marker

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18
Q

Does promoting a high fat diet affect LDL particle size? And if so, how?

A

Increases diameter of LDL particle

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19
Q

Does sugar affect LDL size? And if so, how?

A

Decreases diameter

Sugar also impairs glucose and lipid metabolism

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20
Q

What enzyme mediates the conversion of O2 to H2O2?

A

Superoxide dismutase

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21
Q

What enzymes convert H2O2 into H2O? Which is most important?

A

Glutathione (GSH)
Catalase

GSH is most important

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22
Q

What happens if you don’t have enough GSH?

A

If you don’t have enough GSH due to excess oxidative stress, you have HO- free radicals floating around that can oxidize LDLs, making them pathogenic

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23
Q

T/F? Antioxidant therapy reduces atherosclerosis development?

A

True.

People with CAD have reduced antioxidant capacity

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24
Q

What is one way that we can increase antioxidant mechanisms?

A

Exercising

Keto diet increases GSH

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25
Q

What enzyme is a key regulator of cholesterol production?

A

HMG CoA Reductase

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26
Q

What two hormones affect cholesterol absorption?

A

Glucagon

Insulin

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27
Q

What is the effect on cholesterol absorption when insulin is high?

A

Increased absorption

Insulin activates HMG CoA Reductase, increasing cholesterol

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28
Q

What is the effect on cholesterol absorption when glucagon is high?

A

Decreased absorption

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29
Q

What are statins? What do they do?

A

HMG CoA Reductase Inhibitors

Prolong life in those with a h/o CV event, but they provide very little primary protection

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30
Q

What are some adverse side effects of statins?

A

Increased risk of adverse events - 40%

  • Increased risk of diabetes
  • – T2DM increased by 50%
  • Kidney failure
  • Liver failure
  • Muscle pain
  • – Rhabdomyolysis may be b/c of reduced ubiquinone (Coenzyme Q10)
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31
Q

What effects does reduced ubiquinone (Coenzyme Q10) manifest? How can you tx this?

A
  • Rhabomyolysis
  • Myopathy (muscle weakness and pain)
  • Reduced mitochondrial function
  • Cataracts

CoQ10 supplementation

32
Q

What is the effect of oxidative stress on the ETC?

A

Reduced ubiquinone (CoQ10) and superoxide stress blocks the flux of electrons to Complex III because CoQ10 shuttles electrons from Complex I to III

33
Q

What is IMT? Can it indicate plaque size?

A

Intima Media Thickness; Yes

Statins have no effect on IMT

34
Q

What is the effect of statins on atherosclerotic plaques and LDL diameter?

A

No effect

35
Q

What is the most cost

effective preventative tx for coronary heart disease?

A

Aspirin

  • 1/5 the cost
  • Better potential tx for atherosclerosis than statin or just as good
  • Helps keep the platelets “slippery”
36
Q

Why is cholesterol important?

A
  • Cell membranes
  • Steroid synthesis
  • Bile salts
  • Vitamin D
  • Ubiquinone
37
Q

What does data suggest about statins and cholesterol?

A
  • Statins reduce risk of a re-occurring CV event
  • Statins are not effective at primary prevention
  • Statins do not reduce overall mortality
  • Stains may elicit significant side effects
38
Q

Atherosclerosis development steps

A
  1. LDL-B enters through the endothelium
  2. LDL-B is oxidized (from ROS)
  3. Oxidized LDL-B attracts macrophages
  4. Macrophages become lipid laden and turn into “foam cells”
  5. Foam cells accumulate and induce inflammation
  6. Plaque consists of foam cells and WBCs
39
Q

What are the different types and causes of hypertension?

A

Benign

  • Essential (95% of cases)
  • Secondary

Malignant

40
Q

What are the two types of benign hypertension and the causes of each?

A
  1. Essential
    - AKA Primary HTN
    - Idiopathic
    - Mix of genetic and environmental factors
    - Erroneously assumed to result from weight gain
  2. Secondary - if you know the cause
    - Results from structural (aortic coarctation), renal (renal artery stenosis), endocrine defect (adrenocortical hyperfunction)
41
Q

What does benign HTN increase the risk of?

A
  • Atherogenesis
  • Aortic dissection
  • Stroke
42
Q

What type of hypertension can cause small blood vessel disease?

A

Benign

43
Q

Types of small BV diseases?

A

Hyaline arteriosclerosis

  • Hyaline = glassy, pink appearance
  • Usually an acellular, protenaceous material

Hyperplastic arteriosclerosis
- Concentric arteries

44
Q

Malignant HTN. What does it usually accompany?

A

Lethal i n 1-2 years if untx’d
>200/120mmHg

  • Renal failure
  • Retinal hemorrhages
  • Papilledema
45
Q

What diseases can primary hypertension: insulin resistance give rise to?

A
  1. RAAS dysfunction
  2. Enhanced GF activity/Endothelial hypertrophy
  3. SNS dysfunction
  4. Dyslipidemia
  5. Reduced nitric oxide
46
Q

What is RAAS dysfunction, induced by primary HTN: insulin resistance?

A

Insulin increases kidney Na+ reabsorption
- Insulin increases aldosterone secretion

Slight increase in plasma insulin is capable of eliciting an antidiuretic effect

*If insulin is high, you’ll have water retention

47
Q

What is endothelial hypertrophy/enhanced GF activity, induced by primary HTN: insulin resistance?

A

Receptors for IGF-1 and insulin in capillary endothelial cells

  • Vascular cells are responsive to insulin
  • Hypertrophy of vascular wall = narrowing of vascular lumen
48
Q

What is SNS dysfunction, induced by primary HTN: insulin resistance?

A

Insulin causes dose-related increase in NE release

- Increase in pulse and BP

49
Q

What is dyslipidemia, induced by primary HTN: insulin resistance?

A
  • Reduced HDL
  • Increased VLDL
  • Increased LDL - pattern B
  • Increased TG
50
Q

What is decreased NO, induced by primary HTN: insulin resistance?

A

NO reduces BP
- Potent vasodilator

Insulin inhibits NO production

  • Insulin resistant endothelial cells fail to release NO
  • Insulin resistance, insulin can’t induce NO-mediated vasodilation
51
Q

What is the major pathogenic defect initiating the hypertensive process?

A

Insulin resistance

52
Q

Salt sensitive HTN

A

Insulin resistance MIGHT explain salt sensitivity, but there may exist a distinct genetic component

53
Q

What is DASH diet and what are its effects on HTN?

A

Diet low in refined carbs, high fruit/veg, low sodium

Decreases BP

54
Q

What is an aneurysm?

A

Localized abnormal BV dilation

55
Q

What are the two types of aneurysms?

A

True
- Involves all three layers

False
- Hole covered with hematoma because of tear in innermost layers

56
Q

What is the most common aneurysm?

A

Abdominal aortic aneurysm.

Males <50

57
Q

What can cause aneurysms?

A 
Atherosclerosis
Wall degeneration
Trauma
Congenital defects (ie Marfans)
Infection
Hypertension
58
Q

What is aortic dissection?

A

Aortic wall tears and blood pours into wall

  • HTN men, 40-60yo
  • Sudden onset, severe pain
  • Can rupture causing massive hemorrhage`
59
Q

Three different types of aortic dissection

A

I. Originates in ascending aorta, propagates at least to the aortic arch and beyond it distally

II. Originates in ascending aorta and confined to ascending aorta

III. Originates in descending, rarely extends proximally, but does distally

60
Q

What are two vasculitis diseases affecting large vessels?

A

Giant cell arteritis

Takayasu arteritis

61
Q

Giant-cell arteritis

A

Large vessel vasculitis.
MOST COMMON

Feature
- Chronic granulomatous inflammation of arteries in the head
- Accompanied by vague (fever) and/or localized (headache, vision loss) symptoms
Tx: Corticosteroids

Related diseases
- None

Summary

  • > 50
  • Arteries in head
62
Q

Takayasu arteritis

A

Large vessel vasculitis.

Feature

  • Granulomatous inflammation of aortic arch
  • Severe narrowing of major branches
  • Ocular disturbances

Related diseases
- None

Summary

  • F<40
  • “Pulseless disease” - weakening of pulse in upper extremities
63
Q

What are the two vasculitis diseases affecting medium vessels?

A

Polyarteritis nodosa

Kawasaki disease

64
Q

Polyarteritis nodosa

A

Medium vessel vasculitis.

Feature

  • Necrotizing vasculitis throughout the body
  • Fatal if untx’d, but steroids are curative

Related diseases
- Hep B Ag-Ab complexes

Summary

  • Young adults
  • Widespread - different stages can coexist in the same artery
65
Q

Kawasaki disease

A

Medium vessel vasculitis.

Feature
- Possibly necrotizing

Related diseases
- None

Summary

  • <4
  • Coronary disease
  • Lymph nodes
66
Q

What are the three vasculitis diseases affecting small vessels?

A

Wegener granulomatosis
Churg-Strauss syndrome
Microscopic polyangitis

67
Q

Wegener granulomatosis

A

Small vessel vasculitis.

Feature

  • Lung granulomas and renal disease
  • Strawberry gingivitis
  • Palatal ulcerations

Related diseases
- Churg-Strauss - typically relates to allergies and asthma

Summary

  • Lung, kidney
  • c-ANCA
68
Q

Churg-Strauss syndrome

A

Small vessel vasculitis.

Feature

  • Vasculitis in lung
  • Triad:
  • – Lung granulomas
  • – Renal disease
  • – Vasculitis
  • Fatal if untx’d (within a year)
  • Similar, but related to allergies and asthma without renal disease
  • T-cell mediated hypersensitivity

Related diseases
- Wegener

Summary

  • Lung
  • Eosinophils
  • Asthma
  • p-ANCA, c-ANCA positive
69
Q

Microscopic polyangitis

A

Small vessel vasculitis.

Feature

  • Vasculitis in lung and kidney
  • Widespread necrotizing vasculitis in smaller vessels
  • Ab response to drug or bug
  • Neutrophils heavily present in vessels
  • Possble Type III hypersensitivity
  • Removed offending agent usually resolves problem

Related diseases
- None

Summary

  • Lung, kidney
  • p-ANCA
70
Q

Tumors

A

Hemangioma
Glomus tumor
Kaposi sarcoma
Angiosarcoma

71
Q

Hemangioma

A

Common benign tumor of BV

72
Q

What are the three types of hemangioma?

A
  1. Capillary
    - Skin, oral mucosa, sometimes organs
    - “Strawberry” type present at birth, regresses
  2. Cavernous
    - Organs, sometimes skin
    - Cosmetic problem, unless brain
  3. Pyogenic
    - Rapidly growing red nodule on skin, in mouth
    - Microscopically resembles granulation tissue
73
Q

Glomus tumor

A
  • Benign but painful
  • Arise from glomus body cells
  • Distal digits, especially under fingernails
  • Excise
74
Q

Kaposi sarcoma

A
  • Low grade malignancy of endothelial cells
  • Four forms
    1. Chronic
    2. African
    3. Transplant associated
    4. AIDS associated
  • Clinical course varies (chronic is best prognosis)
  • Excise
75
Q

Angiosarcoma

A
  • High grade malignancy of endothelial cells
  • Often in skin, soft tissue, breast, liver
  • Arsenic and PVC increase risk
  • Covers a spectrum from well-differentiated to anaplalstic
  • Metastasize rapidly: 30% survival at 5 years

DMD 5247 (7 decks)

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