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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
Q

What does sclerosis mean?

A

Collagen deposition

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26
Q

Malignant (Accelerated) HTN

A

> 200 and > 120 causing end organ damage

Headache and dramatic elevations of BP, which get worse as times goe by

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27
Q

Malignant (Accelerated) HTN: Medical Emergency

A

Untreated patients die with 2 years from renal failure, intra-cerebral hemorrhage or CHF

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28
Q

Malignant (Accelerated) HTN: Morphology of Kidney (S16)

A

Petechial hemorrhages (Flea-bitten appearance)

Small red spots in kidney

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29
Q

Malignant (Accelerated) HTN: Microscopy of Kidney (S16)

A

Hyperplastic arteriosclerosis (onion skin)

Necrotizing arteriolitis (Fibrinoid necrosis of vessel walls)

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30
Q

Arteriosclerosis (Hardening of Arteries) and 3 Patterns

A

Thickening and loss of elasticity of arterial walls

Patterns

  1. Atherosclerosis
  2. Hypertensive arteriosclerosis
  3. Monckeberh’s medial calcific stenosis
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31
Q

Atherosclerosis is a

A

Form of arteriosclerosis of the intima of large blood vessels characterized by formation of fibro fatty plaques called atheroma

32
Q

Atherosclerosis Common Sites (6)

A

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
Q

Atherosclerosis: Major Non-Modifiable (4)

A

Increasing Age

Male Gender

Family History

Genetic abnormalities - familial hypercholesterolemia

34
Q

Atherosclerosis: Lesser, Uncertain, or Non-Quantitated (5)

A

Obesity

Physical inactivity

Stress (Type A Personality)

Postmenopausal estrogen deficiency

High Carb intake

35
Q

Atherosclerosis: Potentially Controllable (7)

A

Hyperlipidemia

Hypertension

Cigarette smoking

Diabetes

Lipoprotein a

Hardened (trans)unsaturated fat intake

Chlamydia pneumoniae

36
Q

Atherosclerosis: Pathogenesis

A

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
Q

Atherosclerosis: Complications

A

Rupture, ulceration, or erosion – aorta below renal artery

37
Q

Atherosclerosis: Complications - Hemorrhage

A

Hematoma → expand plaque / induce plaque rupture

38
Q

Atherosclerosis: Complications - Superimposed Thrombosis

A

On disrupted lesions (rupture, ulceration, erosion, or hemorrhage) → occlude lumen

39
Q

Atherosclerosis: Complications - Aneurysmal Dilation

A

Weakness and Rupture

40
Q

Atherosclerosis: Complications - Primary pathogenesis of?

A

IHD, MI, or Aneurysms

41
Q

Atherosclerosis: Complications - CNS Disease

A

TIA, Stroke, Atrophy

42
Q

Atherosclerosis: Complications - Peripheral Vascular Disease

A

Claudication or amputation of an extremity

43
Q

Atherosclerosis: Complications - Kidney Failure

A

Reno-vascular hypertension or kidney infarction

44
Q

Atherosclerosis: Complications - GI Disease

A

Mesenteric Angina

Bowel Infarction

Ischemic Strictures

45
Q

Atherosclerosis: Monckeberg’s arteriosclerosis

A

Dystrophic calcification of media of small & medium sized vessels in persons > 50 yrs
Clinically insignificant degenerative disease

46
Q

Atherosclerosis: Monckeberg’s arteriosclerosis

A

Dystrophic calcification of media of small & medium sized vessels in ELDERLY

Clinically insignificant degenerative disease

47
Q

Atherosclerosis: Monckeberg’s arteriosclerosis - Sites (5)

A
  1. Femoral
  2. Tibial
  3. Radial
  4. Ulnar
  5. Genital Arteries
48
Q

Monckeberg’s arteriosclerosis - Microscopy and Lab (3)

A
  1. Deposits of calcium in the tunica media (dystrophic calcification)
  2. No inflammatory reaction seen (Slide 33)
  3. X-ray done after falling
49
Q

Monckeberg’s arteriosclerosis - Microscopy (2)

A
  1. Deposits of calcium in the tunica media (dystrophic calcification)
  2. No inflammatory reaction seen (Slide 33)
50
Q

Atherosclerosis is in?

A

Below origin of renal artery bifurcation in abdominal aorta is most common site

51
Q

Aneurysm: Defined

A

Localized abnormal dilation of blood vessel or wall of heart in THORACIC AORTA

52
Q

Aneurysm: Types (2)

A
  1. Saccular (spherical)

2. Fusiform (spindle shaped)

53
Q

Aneurysm: Most Common Etiologies (2 causes)

A
  1. In ascending aorta
    • Dissecting aortic aneurysm proximally
    • Hypertension
  2. In distal aorta (thoracic and abdominal) AND IN EXTREMITIES
    • Atherosclerosis
54
Q

Aneurysm: Causes (4 points)

A

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
Q

Aneurysm: Types (3)

A
  1. Saccular (spherical)

2. Fusiform (spindle shaped)

57
Q

Abdominal Aortic Aneurysms: Cause SITE Age, and Sex

A

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
Q

Abdominal Aortic Aneurysms: Cause

A

Intrinsic/acquired defect in structural components of wall

59
Q

Abdominal Aortic Aneurysms: Symptoms (2)

A

Asymptomatic or a pulsatile mass (aggressive tx if more than 5 cm)

Mid-abd to lower back pain

60
Q

Abdominal Aortic Aneurysms: Signs (1)

A

Abdominal bruit on auscultation (50%)

61
Q

Abdominal Aortic Aneurysms: Complications (2)

A
  1. Rupture (most common)

2. C/F - Abrupt severe back pain: **Decreased BP

62
Q

Abdominal Aortic Aneurysms: Lab

A

Abdominal Ultrasound

63
Q

Syphilitic Aneurysm: Defined (2)

A

Tertiary stage of syphilis

Obliterative endarteritis of vasa vasorum and aortitis

64
Q

Syphilitic Aneurysm: Site

A

Thoracic Aota

65
Q

Syphilitic Aneurysm: Gross

A

“Tree barking” - Intimal roughening

66
Q

Syphilitic Aneurysm: Complications (3)

A
  1. Rupture
  2. Aortic insufficiency
  3. Narrowing of coronary ostia
67
Q

Berry Aneurysm: Site (2)

A
  1. Cerebral Artery at bifurcations of Circle of Willis

2. **Anterior Communicating Artery with ACerebralA

68
Q

Berry Aneurysm: Cause (2)

A
  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
Q

Berry Aneurysm: Complication

A

Rupture –> subarachboid hemorrhage, i.e. ‘worst headache of my life’

69
Q

Aortic Dissection: Definition

A

Entry of blood from vessel lumen enters an intimal tearand dissects through layers of media

Slide 45 - splitting of tunica media

70
Q

Aortic Dissection: Etiology (2)

A
  1. Degeneration (cystic medial necrosis) of tunica media

2. Loss of elastic and smooth muscle fibers

71
Q

Aortic Dissection: Proximal (Type A) Lesions (2)

A

Dissections within 1st 10 cm of proximal aorta (ascending aorta)

Most common; most dangerous

72
Q

Aortic Dissection: Predisposing Factors (2)

A
  1. **Hypertension

2. **Marfan’s Syndrome (fibrillin defect)

73
Q

Aortic Dissection: Type B Lesions (3)

A

Dissections that don’t involve ascending aorta

Begin below sub-clavian artery

Less common, better prognosis

74
Q

Aortic Dissection: Symptoms (2)

A
  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
Q

Aortic Dissection: Labs (3)

A
  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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