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”
2
Q
Vessels most affected by Atherosclerosis
A
- Abdominal aorta
- Coronary arteries
- Popliteal arteries
- Carotid arteries
- Vessels of the circle of Willis
3
Q
Layers of Plaque
A
Fibrous Cap
Lipid Core
Necrotic Center (foam cells)
Tunica Media
4
Q
Lipid Core in Plaque mainly
A
mainly cholesterol and cholesterol esters
5
Q
More people are gettting _____ but fewer people are
A
CVD, dying
6
Q
LDL cholesterol types
A
A type: large and less dense
B type: small, more dense
7
Q
which LDL cholesterol type easily penetrates endothelium?
A
Patteren B
8
Q
Risk factors for Pattern B
A
Genetics
Oral contraceptives
Diet
9
Q
Pattern B can be measured by using
A
LDL-S3 GGE test
berkely test
10
Q
Pattern B cholestrolincreased/induced by
A
- very low fat and high carb diet
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)
12
Q
Extremely low-fat diets can
A
increase heart disease risk in some
13
Q
LDL particle size _______ with low carb diet
A
increased
14
Q
Besides dietary fat, what else alters blood lipids?
A
sugar
15
Q
what must occur for cholesterol to be a pathogenic?
A
Oxidation
16
Q
Atherosclerosis steps
5
A
- LDL enters intima through intact endothelium
- Intimal LDL is oxidixed into proinflamitory lipids
- Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across endothelium
- Monocytes differentiate into macrophages and then consume large amounts of LDL –> foam cells
- Foam cells release growth factors (cytokines) that encourage atherosclerosis
17
Q
Antioxidant therapy
A
reduces atherosclerosis plaque development
18
Q
People with CAD have
cornary artery disease
A
reduced antioxidant capacity
19
Q
what increased antioxidant mechanisms ?
SOD
A
exercise
20
Q
Most circulating cholesterol is synthesized
A
de novo
21
Q
Statins inhibits
A
HMG-CoA reductase
22
Q
Statins problems
A
- increase risk of diabetes (50%)
- adverse events risk (40% )
- little primary protection
23
Q
Statins adverse risks
A
diabetes
kidney failure
liver failure
muscle pain
cataracts
24
Q
muscle pain and statins
A
Rhabdomyolysis= muscle break down
(beacause reduced ubiquinone in ETC )
25
The most effective preventive treaments to coronart heart disease prevention is \_\_\_\_\_\_
aspirin
26
Important functins of cholesterol
cell membranes
steroid synthesis
bile salts
vitamin D
Ubiquinone
27
Bickmen Atherosclerosis Steps (6)
## Footnote
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
28
Hypertension is usually
asymptomatic
29
Hypertension table
(vaules)
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
30
What are the different causes of Hypertension ?
Benign
* essential (95% of cases)- other cause
* Secondary-
Malignant
31
Types of Benign Hypertension
Essential
Secondary
32
Benign Essential
* aka primary hypertension
* idiopathic
* mix of genetic and environmental factors
* Erroneously assumed to result from weight gain
due to other cause
33
Benign Secondary Hypertension
structural= aortic coarctation
rental defect= rental artery stenosis
endocrine defect= adrenocorticol hyperfunction
34
Benign Hypertention increases the risk of
atherogenesis
aortic dissection
stroke
35
Benign Hypertension causes small blood vessel diseases such as
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis
36
Hyaline arteriosclerosis
glassy, pink appearance
usually an acellular, proteiaceous material
Benign Hypertension
37
Hyperplastic arteriosclerosis
concentric arteries
Benign Hypertention--\> small blood vessel disease
38
Malignant Hypertension
lethal in 1-2 years if untreated
\>200/120 mmHg
39
Malignant Hypertension usually accompanies
Renal Failure
Retinal hemorrhages
Papilledema (swelling in the eye)
40
Primary Hypertension : Insulin Resistance (increase)
RAAS Dysfunction
* increases kidney sodium reabsorption
* increases aldosterone secretion (retention of water)
41
increase in plasma insulin can cause
antidiuretic effect
(water retention in the blood--\> increaes blood pressure)
42
Where are receptors for IGF-1 and insulin located ?
what does this cause?
in capillary endothelial cells
vascular cells very responsive to insulin --\>Hypertropy
43
Hypertrophy of the vasular wall leads to
narowing of vascular lumen
44
insulin causes a dose-related increase in norepinephrine release which leads to
increase in pulse and blood pressure
45
Insulin resistance and Primary hypertenion
* Reduces HDL
* Increased VLDL
* Increased LDL-patteren B
* Increased TG
46
Nitiric Oxide _______ BP beacuse it is a potent \_\_\_\_\_\_\_\_
reduces
vasodilator
47
\_\_\_\_\_\_ increase production of edothelium derived NO
Insulin
48
Insulin resistant endothelial cells can't release NO which is unable to induce \_\_\_\_\_\_\_\_\_\_\_
NO- mediated vasodilation
49
Aneurysm
localized abnormal vessel dilation
50
What are the two types of aneurysms?
True
False
51
True aneurysms
invilve all three layers of the vessel
52
false aneurysms
hole covered with hematoma on vessel
53
Abdominal aortic aneurysm causes
* males \>50
Can be caused by
* Atherosclerosis
* Wall degeneration
* Trauma
* Congenital defects (e.g., Marfan)
* Infection
54
Aortic DIssection
aortic wall tears and blood pours into wall
* Hypertensive men, 40-60 yrs
* Sudden onset, severe pain
* Can rupture, causing massive hemorrhage
55
Type I Aortic Dissection
Originates in ascending aorta,
propagates at least to the aortic arch and often beyond it distally.
56
Type II Aortic Dissection
orginates in ascending aorta and is confined to the ascending aorta
57
Type III Aortic DIssection
orginates in descending aorta
rarely extends proximally but will extend distally
58
Aortic DIssection can be caused by
Hypertension
Trauma
59
Vasculitis
inflammation of blood vessels
60
Giant-Cell arteries
Large Vessel
* inflammation of arteries in the head
* \>50
* Most common
* Chronic granulmatous inflammation
* vague (fever)
* localized (headache, vision loss)
61
treatment of giant-cell arteries
corticosteroids
62
Takayasu arteries
Pulseless disease
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
Polyarteritis nodosa
Medium Vessel
* Necrotizing vasulitis throughout the body
* Hep B antigen antibody complexes
* Young adults
* fatal if untreated
64
Polyarteritis nodosa treatment
steroids
65
Wegener granulmotis
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
Common manifestations of Wegener granulomatosis
strawberry gingivitis (common)
Palatal Ulcerations (rare)
67
Churs-Strauss Syndrome
* Vasculitis in the lung
* Lung.
* Eosinophil
* Asthma.
* p-ANCA.
* **Similar to Wegener G, but related to allergies and asthma, without renal disease**
68
what two small vessel diseases are related to each other ?
Wengener granulomatois
and
Churg-Strauss syndrome
69
Microscopic polyangiitis
* 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
Aortic Dissection
types A and B
Aortic Dissection
Type A starts in Ascending
Type B starts in the descending aorta
71
What usually solves the problem of Microscopic polyangiitis ?
removing offending agent usually resolves problem
72
Hemangioma
types
very common benign tumor of blood vessel
1. Capillary hemagioma
2. Cavernous hemangioma
3. Pyogenic granuloma
73
Capillary Hemangioma
Hemangioma
* Skin, oral mucosa, sometimes organs
* “Strawberry” type present at birth, regresses
74
Cavernous hemangioma
Hemangioma
* Organs, sometimes skin
* Cosmetic problem (unless in the brain)
75
Pyogenic granuloma
Hemangioma
* Rapidly growing red nodule on skin, in mouth
* Microscopically resembles granulation tissue
76
Glomus Tumor
* Benign but painful
* Arise from glomus body cells
* Distal digits, especially under fingernails
* Excise!
77
Kaposi Sarcoma
**Low-grade malignancy of endothelial cells**
Four forms
1. Chronic (older Ashkenazi Jewish males)
2. African
3. Transplant associated
4. AIDS associated
78
What form of Kaposi sarcoma has the best prognosis
chronic
79
Angiosacroma
* 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
What are complicaitons of atherosclerosis?
Stenosis
Thrombosis/embolus
Aneurysm
Calcification
81
where does the creation of ROS occur?
Mitochondria
82
SOD
antioxidant enzyme
converts O2 into peroxide
83
what is the rate limiting enzyme of cholestrol
HMG CoA reductase
84
where is the majority of cholesterol made?
liver
85
what happen if there was an increase of glucagon in the body?
decrease in cholestrol made
incactive HMG CoA reductase
86
what happens if insulin is high in the body for cholestrol prodiuiction
increase cholestrol produciton
activate HMG CoA Reductase
87
common cause of endothelial injury
hypertension
hyperlipidemia
smoking
toxins
viruses
88
Which disease is associated ctANCA ?
Wenger granulmotis
89
why does oxidizing cholestrol make it a problem?
because the macrophages now flagged it as a pathogen and try to engolf it
90
what are some consquences of having too little cholesterol?
ubiquinone is made from cholestrol without it in the ETC you have more O2 radicals
91
If you get a transplant from someone who has HPV 8 or AIDS
more at risk of karposi sarcoma
