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M3 Path Block 2 > 8 - Blood Vessels > Flashcards

8 - Blood Vessels Flashcards

1
Q

The Aortic bifurcation before renal arteries has?

A

Vasovasorum

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2
Q

What part of the vein is thicker in veins compared to arteries?

A

Adventitia

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3
Q

Conditions where veins get dilated?

A

Varicose veins

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4
Q

Consequences of Vascular Disease: Narrowing and Obstruction of the Vessel Lumen

A

Progressively - by atherosclerosis

Precipitously by thrombosis/embolism –> tissue atrophy or infarction

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5
Q

Consequences of Vascular Disease: Weakening of Vessel Wall

A

Leads to dilation (aneurysmal, thrombosis formation), dissection (aortic), or rupture

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6
Q

Congenital Anomalies (2)

A
  1. Anomalous/Variations (unexpected location of vessels)
  2. Berry Aneurysms (saccular)
    - Vascualr out-pouchings (Circle of Willis, ACA)
  • Due to congenital wall weakness
  • Location - cerebral vessels
  • May rupture suddenly - subarachnoid hemorrhage, can cause death immediately
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7
Q

Arterio-Venous (AV) Fistulas

A

Abnormal communications b/w arteries and veins

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8
Q

Arterio-Venous (AV) Fistulas: Etiology

A

Acquired: Dialysis patients (DM and Renal HTN)

Paget’s disease of bone: Increased AV connections in bone

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9
Q

Arterio-Venous (AV) Fistulas: Potential Complications

A

High output heart failure: Large AV fistulas reduce systemic resistance and bypass microcirculation –> increases VR to heart

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10
Q

Hypertension: Idiopathic (Essential) Primary is what percentage?

A

95% of patients, cause unknown

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11
Q

Hypertension: Secondary Hypertension percentage?

A

5% and due to secondary causes

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12
Q

Secondary HTN Causes: Renal Disease

A

Most important secondary cause

Acute glomerulonephritis (Post-streptococcal GN)

Chronic Renal Disease

Polycystic Kidney Disease

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13
Q

Secondary HTN Causes: Endocrine

A

Cushing Syndrome (increased? corticosteroids)

Estogen (including PIH, OCPs), glucocorticoids, MAOIs

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14
Q

Secondary HTN Causes: Cardiovascular

A

Coarctation of aorta

Polyarteritis nodosa (or other vasculitis)

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15
Q

Factors Influencing Development of HTN: Genetic Defects

A

Increased smooth muscle contraction –> increase in TPR

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16
Q

Factors Influencing Development of HTN: Reduced Renal Sodium Excretion

A

Sodium retention –> increase in ECF volume –> increases CO –> increases TPR

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17
Q

Factors Influencing Development of HTN: Activation of RAA System

A

Increases CO and TPR

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18
Q

Factors Influencing Development of HTN: Medications

A

Decongestants

NSAIDs (block vasodilator effect of PG)

Estrogen (increase angiotensinogen synthesis in liver)

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19
Q

HTN: 2 types of Clinical Manifestations

A
  1. Asymptomatic

2. Symptomatic

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20
Q

Symptomatic HTN: Signs

A

Hypertensive Retinopathy

Increased PMI from LVH and S4 sound

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21
Q

Symptomatic HTN: Heart

A

Concentric left ventricular hypertrophy –> congestive cardiac failure, and MI

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22
Q

Symptomatic HTN: Brain

A

Intra-cerebral hemorrhage

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23
Q

Symptomatic HTN: Kidney

A

Chronic renal failure

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24
Q

Vascular Pathology (Slide 14) - 2 Types

A
  1. Hyaline arteriosclerosis

2. Hyperplastic arteriosclerosis (onion skinning)

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25
What does sclerosis mean?
Collagen deposition
26
Malignant (Accelerated) HTN
> 200 and > 120 causing end organ damage Headache and dramatic elevations of BP, which get worse as times goe by
27
Malignant (Accelerated) HTN: Medical Emergency
Untreated patients die with 2 years from renal failure, intra-cerebral hemorrhage or CHF
28
Malignant (Accelerated) HTN: Morphology of Kidney (S16)
Petechial hemorrhages (Flea-bitten appearance) Small red spots in kidney
29
Malignant (Accelerated) HTN: Microscopy of Kidney (S16)
Hyperplastic arteriosclerosis (onion skin) Necrotizing arteriolitis (Fibrinoid necrosis of vessel walls)
30
Arteriosclerosis (Hardening of Arteries) and 3 Patterns
Thickening and loss of elasticity of arterial walls Patterns 1. Atherosclerosis 2. Hypertensive arteriosclerosis 3. Monckeberh's medial calcific stenosis
31
Atherosclerosis is a
Form of arteriosclerosis of the intima of large blood vessels characterized by formation of fibro fatty plaques called atheroma
32
Atherosclerosis Common Sites (6)
In decreasing order 1. Abdominal aorta below renal artery bifurcation 2. Coronary artery - MI 3. Popliteal artery - Peripheral vascular disease 4. Descending thoracic aorta 5. Internal carotid artery - elderly, diffuse generalized atrophy 6. Circle of Willis
33
Atherosclerosis: Major Non-Modifiable (4)
Increasing Age Male Gender Family History Genetic abnormalities - familial hypercholesterolemia
34
Atherosclerosis: Lesser, Uncertain, or Non-Quantitated (5)
Obesity Physical inactivity Stress (Type A Personality) Postmenopausal estrogen deficiency High Carb intake
35
Atherosclerosis: Potentially Controllable (7)
Hyperlipidemia Hypertension Cigarette smoking Diabetes Lipoprotein a Hardened (trans)unsaturated fat intake Chlamydia pneumoniae
36
Atherosclerosis: Pathogenesis
Endothelial injury leading towards endothelial cell dysfunction, which Leads to vascular permeability, causing Leukocyte adhesion, which leads to Cytokine release, then LDL and cytokines combine and form oxidized LDL Blood Monocytes get attracted and get converted to macrophages, which ingest oxidized LDL and become known as foam cells Plateles aggregate due to injured endothelial --> release PDGF, which will induce smooth muscle cell proliferation Oxidized LDL + smooth muscle cell proliferation from PDGF secreted by platelets --> form plaque Last cell to arrive is T cell after plaque formation
37
Atherosclerosis: Complications
Rupture, ulceration, or erosion – aorta below renal artery
37
Atherosclerosis: Complications - Hemorrhage
Hematoma → expand plaque / induce plaque rupture
38
Atherosclerosis: Complications - Superimposed Thrombosis
On disrupted lesions (rupture, ulceration, erosion, or hemorrhage) → occlude lumen
39
Atherosclerosis: Complications - Aneurysmal Dilation
Weakness and Rupture
40
Atherosclerosis: Complications - Primary pathogenesis of?
IHD, MI, or Aneurysms
41
Atherosclerosis: Complications - CNS Disease
TIA, Stroke, Atrophy
42
Atherosclerosis: Complications - Peripheral Vascular Disease
Claudication or amputation of an extremity
43
Atherosclerosis: Complications - Kidney Failure
Reno-vascular hypertension or kidney infarction
44
Atherosclerosis: Complications - GI Disease
Mesenteric Angina Bowel Infarction Ischemic Strictures
45
Atherosclerosis: Monckeberg’s arteriosclerosis
Dystrophic calcification of media of small & medium sized vessels in persons > 50 yrs Clinically insignificant degenerative disease
46
Atherosclerosis: Monckeberg’s arteriosclerosis
Dystrophic calcification of media of small & medium sized vessels in ELDERLY Clinically insignificant degenerative disease
47
Atherosclerosis: Monckeberg’s arteriosclerosis - Sites (5)
1. Femoral 2. Tibial 3. Radial 4. Ulnar 5. Genital Arteries
48
Monckeberg’s arteriosclerosis - Microscopy and Lab (3)
1. Deposits of calcium in the tunica media (dystrophic calcification) 2. No inflammatory reaction seen (Slide 33) 3. X-ray done after falling
49
Monckeberg’s arteriosclerosis - Microscopy (2)
1. Deposits of calcium in the tunica media (dystrophic calcification) 2. No inflammatory reaction seen (Slide 33)
50
Atherosclerosis is in?
Below origin of renal artery bifurcation in abdominal aorta is most common site
51
Aneurysm: Defined
Localized abnormal dilation of blood vessel or wall of heart in THORACIC AORTA
52
Aneurysm: Types (2)
1. Saccular (spherical) | 2. Fusiform (spindle shaped)
53
Aneurysm: Most Common Etiologies (2 causes)
1. In ascending aorta - Dissecting aortic aneurysm proximally - Hypertension 2. In distal aorta (thoracic and abdominal) AND IN EXTREMITIES - Atherosclerosis
54
Aneurysm: Causes (4 points)
Weakened vessel wall due to 1. Congenital defect (Marfan's Ehlers-Danlos) 2. Acquired - Atherosclerosis - Systemic Disease (HTN) Can get aneurysms if there's vitamin C deficient
56
Aneurysm: Types (3)
1. Saccular (spherical) | 2. Fusiform (spindle shaped)
57
Abdominal Aortic Aneurysms: Cause SITE Age, and Sex
Due to atherosclerosis SITE: **Below renal arteries, but above abdominal aorta bifurcation*** There is a lack of vasa vasorum below renal artery orifices > 50 years M:F = 5:1
58
Abdominal Aortic Aneurysms: Cause
Intrinsic/acquired defect in structural components of wall
59
Abdominal Aortic Aneurysms: Symptoms (2)
Asymptomatic or a pulsatile mass (aggressive tx if more than 5 cm) Mid-abd to lower back pain
60
Abdominal Aortic Aneurysms: Signs (1)
Abdominal bruit on auscultation (50%)
61
Abdominal Aortic Aneurysms: Complications (2)
1. Rupture (most common) | 2. C/F - Abrupt severe back pain: **Decreased BP
62
Abdominal Aortic Aneurysms: Lab
Abdominal Ultrasound
63
Syphilitic Aneurysm: Defined (2)
Tertiary stage of syphilis Obliterative endarteritis of vasa vasorum and aortitis
64
Syphilitic Aneurysm: Site
Thoracic Aota
65
Syphilitic Aneurysm: Gross
"Tree barking" - Intimal roughening
66
Syphilitic Aneurysm: Complications (3)
1. Rupture 2. Aortic insufficiency 3. Narrowing of coronary ostia
67
Berry Aneurysm: Site (2)
1. Cerebral Artery at bifurcations of Circle of Willis | 2. **Anterior Communicating Artery with ACerebralA
68
Berry Aneurysm: Cause (2)
1. Congenital - absence of internal elastic lamina and muscular wall 2. Associated with: - PCKD (10-15%) - Coarctation of aorta (Increased pressure in cerebral vessels)
68
Berry Aneurysm: Complication
Rupture --> subarachboid hemorrhage, i.e. 'worst headache of my life'
69
Aortic Dissection: Definition
Entry of blood from vessel lumen enters an *intimal tear*and dissects through layers of media Slide 45 - splitting of tunica media
70
Aortic Dissection: Etiology (2)
1. Degeneration (cystic medial necrosis) of tunica media | 2. Loss of elastic and smooth muscle fibers
71
Aortic Dissection: Proximal (Type A) Lesions (2)
Dissections within 1st 10 cm of proximal aorta (ascending aorta) Most common; most dangerous
72
Aortic Dissection: Predisposing Factors (2)
1. **Hypertension | 2. **Marfan's Syndrome (fibrillin defect)
73
Aortic Dissection: Type B Lesions (3)
Dissections that don't involve ascending aorta Begin below sub-clavian artery Less common, better prognosis
74
Aortic Dissection: Symptoms (2)
1. Severe Tearing Pain - Acute onset chest pain; radiates to back 2. *May compress and obstruct aortic branches (e.g. Renal, Mesenteric, and Coronary Arteries)
76
Aortic Dissection: Labs (3)
1. Chest X-Ray - mediastinal widening 2. Retrograde arteriography (gold standard) Slide 48 - Double Barrel Aorta

M3 Path Block 2 (10 decks)

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