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DMD 5247 > Blood Vessel Pathology-Bickmen > Flashcards

Blood Vessel Pathology-Bickmen Flashcards

1
Q

Atherosclerosis

A
  • The most common form of arteriosclerosis
  • Atherosclerotic plaque
    • “A narrowing and hardening of arteries due to intimal athermonas”
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2
Q

Vessels 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

Layers of Plaque

A

Fibrous Cap

Lipid Core

Necrotic Center (foam cells)

Tunica Media

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4
Q

Lipid Core in Plaque mainly

A

mainly cholesterol and cholesterol esters

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5
Q

More people are gettting _____ but fewer people are

A

CVD, dying

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6
Q

LDL cholesterol types

A

A type: large and less dense

B type: small, more dense

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7
Q

which LDL cholesterol type easily penetrates endothelium?

A

Patteren B

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8
Q

Risk factors for Pattern B

A

Genetics

Oral contraceptives

Diet

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9
Q

Pattern B can be measured by using

A

LDL-S3 GGE test

berkely test

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10
Q

Pattern B cholestrolincreased/induced by

A
  • very low fat and high carb diet
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11
Q

LDL-B measured in blood

What is the best indicator

more commons measure

A
  • not measured
  • TG:HDL best indicator (ideal<1.5)
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12
Q

Extremely low-fat diets can

A

increase heart disease risk in some

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13
Q

LDL particle size _______ with low carb diet

A

increased

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14
Q

Besides dietary fat, what else alters blood lipids?

A

sugar

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15
Q

what must occur for cholesterol to be a pathogenic?

A

Oxidation

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16
Q

Atherosclerosis steps

5

A
  1. LDL enters intima through intact endothelium
  2. Intimal LDL is oxidixed into proinflamitory lipids
  3. Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across endothelium
  4. Monocytes differentiate into macrophages and then consume large amounts of LDL –> foam cells
  5. Foam cells release growth factors (cytokines) that encourage atherosclerosis
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17
Q

Antioxidant therapy

A

reduces atherosclerosis plaque development

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18
Q

People with CAD have

cornary artery disease

A

reduced antioxidant capacity

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19
Q

what increased antioxidant mechanisms ?

SOD

A

exercise

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20
Q

Most circulating cholesterol is synthesized

A

de novo

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21
Q

Statins inhibits

A

HMG-CoA reductase

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22
Q

Statins problems

A
  1. increase risk of diabetes (50%)
  2. adverse events risk (40% )
  3. little primary protection
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23
Q

Statins adverse risks

A

diabetes

kidney failure

liver failure

muscle pain

cataracts

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24
Q

muscle pain and statins

A

Rhabdomyolysis= muscle break down

(beacause reduced ubiquinone in ETC )

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25
Q

The most effective preventive treaments to coronart heart disease prevention is ______

A

aspirin

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26
Q

Important functins of cholesterol

A

cell membranes

steroid synthesis

bile salts

vitamin D

Ubiquinone

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27
Q

Bickmen Atherosclerosis Steps (6)

A

  1. LDL-B enters through the endothelium
  2. LDL-B is oxidized (from ROS) by mitochcondria
  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 white blood cells
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28
Q

Hypertension is usually

A

asymptomatic

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29
Q

Hypertension table

(vaules)

A

Systolic pressure Diastolic pressure

Normal 90–119 60–79

Prehypertension 120–139 80–89

Stage 1 hypertension 140–159 90–99

Stage 2 hypertension ≥160 ≥100

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30
Q

What are the different causes of Hypertension ?

A

Benign

  • essential (95% of cases)- other cause
  • Secondary-

Malignant

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31
Q

Types of Benign Hypertension

A

Essential

Secondary

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32
Q

Benign Essential

A
  • aka primary hypertension
  • idiopathic
  • mix of genetic and environmental factors
  • Erroneously assumed to result from weight gain

due to other cause

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33
Q

Benign Secondary Hypertension

A

structural= aortic coarctation

rental defect= rental artery stenosis

endocrine defect= adrenocorticol hyperfunction

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34
Q

Benign Hypertention increases the risk of

A

atherogenesis

aortic dissection

stroke

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35
Q

Benign Hypertension causes small blood vessel diseases such as

A

Hyaline arteriosclerosis

Hyperplastic arteriosclerosis

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36
Q

Hyaline arteriosclerosis

A

glassy, pink appearance

usually an acellular, proteiaceous material

Benign Hypertension

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37
Q

Hyperplastic arteriosclerosis

A

concentric arteries

Benign Hypertention–> small blood vessel disease

38
Q

Malignant Hypertension

A

lethal in 1-2 years if untreated

>200/120 mmHg

39
Q

Malignant Hypertension usually accompanies

A

Renal Failure

Retinal hemorrhages

Papilledema (swelling in the eye)

40
Q

Primary Hypertension : Insulin Resistance (increase)

A

RAAS Dysfunction

  • increases kidney sodium reabsorption
  • increases aldosterone secretion (retention of water)
41
Q

increase in plasma insulin can cause

A

antidiuretic effect

(water retention in the blood–> increaes blood pressure)

42
Q

Where are receptors for IGF-1 and insulin located ?

what does this cause?

A

in capillary endothelial cells

vascular cells very responsive to insulin –>Hypertropy

43
Q

Hypertrophy of the vasular wall leads to

A

narowing of vascular lumen

44
Q

insulin causes a dose-related increase in norepinephrine release which leads to

A

increase in pulse and blood pressure

45
Q

Insulin resistance and Primary hypertenion

A
  • Reduces HDL
  • Increased VLDL
  • Increased LDL-patteren B
  • Increased TG
46
Q

Nitiric Oxide _______ BP beacuse it is a potent ________

A

reduces

vasodilator

47
Q

______ increase production of edothelium derived NO

A

Insulin

48
Q

Insulin resistant endothelial cells can’t release NO which is unable to induce ___________

A

NO- mediated vasodilation

49
Q

Aneurysm

A

localized abnormal vessel dilation

50
Q

What are the two types of aneurysms?

A

True

False

51
Q

True aneurysms

A

invilve all three layers of the vessel

52
Q

false aneurysms

A

hole covered with hematoma on vessel

53
Q

Abdominal aortic aneurysm causes

A
  • males >50

Can be caused by

  • Atherosclerosis
  • Wall degeneration
  • Trauma
  • Congenital defects (e.g., Marfan)
  • Infection
54
Q

Aortic DIssection

A

aortic wall tears and blood pours into wall

  • Hypertensive men, 40-60 yrs
  • Sudden onset, severe pain
  • Can rupture, causing massive hemorrhage
55
Q

Type I Aortic Dissection

A

Originates in ascending aorta,

propagates at least to the aortic arch and often beyond it distally.

56
Q

Type II Aortic Dissection

A

orginates in ascending aorta and is confined to the ascending aorta

57
Q

Type III Aortic DIssection

A

orginates in descending aorta

rarely extends proximally but will extend distally

58
Q

Aortic DIssection can be caused by

A

Hypertension

Trauma

59
Q

Vasculitis

A

inflammation of blood vessels

60
Q

Giant-Cell arteries

A

Large Vessel

  • inflammation of arteries in the head
  • >50
  • Most common
  • Chronic granulmatous inflammation
  • vague (fever)
  • localized (headache, vision loss)
61
Q

treatment of giant-cell arteries

A

corticosteroids

62
Q

Takayasu arteries

Pulseless disease

A

Large Vessel

  • Inflammation of aortic arch
  • F<40
  • Granulomatous vasculitis of the aortic arch
  • Severe narrowing of major branches
  • Weakening of pulse in upper extremities
  • Ocular disturbances
63
Q

Polyarteritis nodosa

A

Medium Vessel

  • Necrotizing vasulitis throughout the body
  • Hep B antigen antibody complexes
  • Young adults
  • fatal if untreated
64
Q

Polyarteritis nodosa treatment

A

steroids

65
Q

Wegener granulmotis

A

small vessel diseae

  • Most commonly affects ~40yrs
  • Triad: Lung granulomas, renal disease, vasculitis
  • c-ANCA positive
  • T-cell mediated hypersensitivity type III
  • Fatal if untreated (within a year)
66
Q

Common manifestations of Wegener granulomatosis

A

strawberry gingivitis (common)

Palatal Ulcerations (rare)

67
Q

Churs-Strauss Syndrome

A
  • Vasculitis in the lung
  • Lung.
  • Eosinophil
  • Asthma.
  • p-ANCA.
  • Similar to Wegener G, but related to allergies and asthma, without renal disease
68
Q

what two small vessel diseases are related to each other ?

A

Wengener granulomatois

and

Churg-Strauss syndrome

69
Q

Microscopic polyangiitis

A
  • Vasculitis in lung and kidney
  • Widespread, necrotizing vasculitis of smaller vessels
  • Antibody response to drug or bug (type III hypersenitivity)
  • Neutrophils heavily present in vessels
70
Q

Aortic Dissection

types A and B

A

Aortic Dissection
Type A starts in Ascending
Type B starts in the descending aorta

71
Q

What usually solves the problem of Microscopic polyangiitis ?

A

removing offending agent usually resolves problem

72
Q

Hemangioma

types

A

very common benign tumor of blood vessel

  1. Capillary hemagioma
  2. Cavernous hemangioma
  3. Pyogenic granuloma
73
Q

Capillary Hemangioma

A

Hemangioma

  • Skin, oral mucosa, sometimes organs
  • “Strawberry” type present at birth, regresses
74
Q

Cavernous hemangioma

A

Hemangioma

  • Organs, sometimes skin
  • Cosmetic problem (unless in the brain)
75
Q

Pyogenic granuloma

A

Hemangioma

  • Rapidly growing red nodule on skin, in mouth
  • Microscopically resembles granulation tissue
76
Q

Glomus Tumor

A
  • Benign but painful
  • Arise from glomus body cells
  • Distal digits, especially under fingernails
  • Excise!
77
Q

Kaposi Sarcoma

A

Low-grade malignancy of endothelial cells
Four forms

  1. Chronic (older Ashkenazi Jewish males)
  2. African
  3. Transplant associated
  4. AIDS associated
78
Q

What form of Kaposi sarcoma has the best prognosis

A

chronic

79
Q

Angiosacroma

A
  • High-grade malignancy of endothelial cells
  • Often in skin, soft tissue, breast, liver
  • Arsenic and PVC increase risk
  • well-differentiated to anaplastic

Metastasize rapidly: 30% survival at 5 yrs

80
Q

What are complicaitons of atherosclerosis?

A

Stenosis
Thrombosis/embolus
Aneurysm
Calcification

81
Q

where does the creation of ROS occur?

A

Mitochondria

82
Q

SOD

A

antioxidant enzyme

converts O2 into peroxide

83
Q

what is the rate limiting enzyme of cholestrol

A

HMG CoA reductase

84
Q

where is the majority of cholesterol made?

A

liver

85
Q

what happen if there was an increase of glucagon in the body?

A

decrease in cholestrol made

incactive HMG CoA reductase

86
Q

what happens if insulin is high in the body for cholestrol prodiuiction

A

increase cholestrol produciton

activate HMG CoA Reductase

87
Q

common cause of endothelial injury

A

hypertension

hyperlipidemia

smoking

toxins

viruses

88
Q

Which disease is associated ctANCA ?

A

Wenger granulmotis

89
Q

why does oxidizing cholestrol make it a problem?

A

because the macrophages now flagged it as a pathogen and try to engolf it

90
Q

what are some consquences of having too little cholesterol?

A

ubiquinone is made from cholestrol without it in the ETC you have more O2 radicals

91
Q

If you get a transplant from someone who has HPV 8 or AIDS

A

more at risk of karposi sarcoma

DMD 5247 (7 decks)

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