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Colin CPR II > PATH - Blood Vessels > Flashcards

PATH - Blood Vessels Flashcards

1
Q

What are the 3 concentric layers of blood vessels?

A

Intima

  • Single layer of endothelial cells
  • Internal elastic lamina demarcates intima from media

Media

  • Arteries well organized concentric layers of smooth muscle
  • Veins haphazard
  • Elastic arteries: high elastin content allows expansion during systole, recoil during diastole
  • Propels blood towards organs
  • Less compliant with increased age, leading to increased systolic BP
  • Muscular arteries: circumferentially oriented smooth muscle
  • Arteriolar smooth muscle contraction = vasoconstriction; relaxation = vasodilation
  • Arterioles: principal point of physiologic resistance to blood flow
  • Resistance to fluid flow is inversely proportional to the fourth power of the radius
  • Halving the diameter increases the resistance 16-fold (small changes in vasoconstriction or vasodilation has profound effects on BP)

Adventitia
- External to media, often separated from media by wide external elastic lamina

  • Vasa vasorum = vessels of the vessels
  • Small arterioles supply O2 to outer media of large arteries
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2
Q

What are the three types of arteries?

A

Large Elastic Arteries

  • Aorta and its major branches
  • Common Carotid, iliac, pulmonary artery

Medium Sized Muscular Arteries

  • Smaller branches of the aorta
  • Coronary, Renal artery

Arterioles
- Within tissues and organs

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3
Q

What are capillaries?

A

Tiny blood vessels with the diameter of an RBC

No media

Sparse, encircling Pericytes (resemble smooth muscle cells)

Site of gas and nutrient exchange

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4
Q

What are important characteristics of veins?

A

Veins are the site of most inflammatory reactions, vascular leakage, and leukocyte exudation

  • Have larger lumens, thinner and less organized walls
  • Contains about 2/3 of the total blood volume
  • Reverse flow due to gravity prevented in the extremities by venous valves
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5
Q

What are some important characteristics of lymphatic vessels?

A

Lymphatic vessels have thin walls that are lined by specialized endothelium

  • Return intestinal tissue fluid and inflammatory cells to the blood stream
  • Transport bacteria etc. and tumor cells = pathway for disease dissemination
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6
Q

Which blood vessel has the greatest role in Blood Pressure regulation?

A

Arterioles

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7
Q

What are the three vascular anomalies?

A

Aneurysm

Arteriovenous malformations (AVM)

Fibromuscular Dysplasia

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8
Q

What is an aneurysm?

A

Localized abnormal dilation of a blood vessel or the heart

  • Not present at birth, but develop over time due to underlying defect in the media of the vessel
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9
Q

What is AVM?

A

Arteriovenous Malformations

  • Arteriovenous shunting: arteries –> veins WTHOUT intervening capillaries
  • Tangle, worm-like vascular channels with prominent pulsatile arteriovenous shunting with high blood flow
  • Large or multiple AVMs may shunt blood from arterial to venous circulation, forces heart to pump additional volume leading to high-output cariac failure
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10
Q

What is fibromuscular dysplasia?

A

Focal irregular thickening in medium and large muscular arteries (renal, carotid, splanchnic, and vertebral vessels)

Usually developmental defect, but can arise from trauma etc.

Beads on a string appearance on angiography

First degree relatives at increased risk

Young women
- NOT associated with oral contraceptives or increased estrogen expression

Can cause aneurysms that can rupture

Cam cause Renovascular HTN if renal arteries are affected

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11
Q

What is a Berry Aneurysm?

A

AKA Saccular Aneurysm

  • Localized abnormal dilation of a blood vessel.
  • 90% of saccular aneurysms found near major branch point of anterior circulation of Circle of Willis
  • Not present at birth, but develop over time due to underlying defect in the media of the vessel
  • Rupture of saccular aneurysm is the most frequent cause of clinically significant Subarachnoid Hemorrhage [SAH]
  • 20-50% die with first rupture
  • Repeat bleeding common in survivors
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12
Q

What is a mycotic aneurysm?

A

Type of aneurysm that can originate from:

o Embolization of a septic embolus (usually as a complication of infective endocarditis)

o An extension of an adjacent suppurative (disease) process

o Circulating organisms directly infecting the arterial wall

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13
Q

What is the stereotypical response of a vessel wall to any insult?

A

Intimal thickening

Associated with endothelial dysfunction or loss

  • Stimulates smoothe muscle cell recruitment and proliferation and associated matrix synthesis
  • Thus intimal thickening (neointimal response)
  • Smooth cell recruitment involves signaling smooth muscle cell migration and proliferation
  • Associated with extracellular matrix synthesis

Healing response results in intimal thickening that may impede blood flow

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14
Q

What are some causes of Endothelial cells Activation?

A 
Turbulent flow
HTN
Cytokines
Complement
Bacterial products
Lipid products
Advanced glycation end products
Hypoxia, acidosis
Viruses
Cigarette smoke
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15
Q

What changes occur to endothelial cell upon activation?

A

Increased expression of procoagulants, adhesion molecules, and proinflammatroy factors

Altered expression of chemokines, cytokines, and growth factors

Express factors that cause smooth muscle contraction and/or proliferation and matrix synthesis
- VEGF

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16
Q

What causes an activated endothelial cell to return to its basal state?

A

Normotension

Laminar Flow

Low levels of growth factors

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17
Q

What changes occur to an endothelial cell upon returning to its basal state?

A

Promotes maintenance of non-thrombotic, nonadhesive surface with appropriate vascular wall smooth muscle tone

18
Q

What is cardiac output?

A

Heart Rate x Stroke Volume

  • Stroke volume - Strongly influenced by Filling pressure
  • Blood volume which is regulated by renal sodium excretion or resorption, mineralocorticoids, and Atrial Natriuretic Peptide (ANP)

Heart rate and Contractility

19
Q

What is vascular resistance?

A

Resistance to blood flow

Regulated at level or arterioles

Influenced by neural and hormonal inputs

20
Q

What is the equation for Blood Pressure?

A

BP = Cardiac Output x Peripheral Resistance

21
Q

What neural factors control cardiac output?

A

Alpha and Beta adrenergic systems regulate fill pressure, heart rate/contractility and peripheral resistance

Alpha adrenergic signaling causes vasoconstriction

Beta adrenergic signaling causes vasodilation

22
Q

What humoral factors induce vasoconstriction?

A

Angiotensin II, Catecholamines (epinephrine/norepinephrine), endothelin

23
Q

What humoral factors induce vasodilation?

A

Kinins, prostaglandins, and nitric oxide (NO)

24
Q

How do blood vessels autoregulate peripheral resistance?

A

Increased blood flow will induce vasoconstriction in vessels as a means to protect tissues against hyperperfusion

BP is fine tunes by tissue pH and hypoxia to accommodate local metabolic demands

25
Q

What is RAAS?

A

Renin-Angiotensin-Aldosterone System

Juxtaglomerular cells in the afferent arterioles of the kidney secrete Renin in response to low blood volume, low peripheral resistance, or decreased glomerualr filtration rate

Renin cleaves circulating angiotensinogen into Angiotensin I

Angiotensin I is cleaved into Angiotensin II by Angiotensin Converting Enzyme (ACE) in the lungs

Angiotensin II is a short-lived, but potent vasoconstrictor

Angiotensin II also signals the Adrenal Cortex to secrete Aldosterone

Aldosterone causes an increase in renal reabsorption of Na+ and H2O

Overall, blood volume and blood pressure are increased

26
Q

What is ANP?

A

Atrial Natriuretic Peptide

It is a hormone released from the myocardium in response to high blood pressure

It promotes Na+ excretion and diuresis, as well as vasodilation

Overall, promotes a decrease in blood pressure and blood volume

27
Q

How does a plaque form?

A

Endothelial injury causes platelet and monocyte adhesion to endothelium.

Monocytes migrate into the intima from the lumen and smooth muscle cells migrate into the intima from the media

Monocytes are activated into Macrophages

Macrophages and smooth muscles cells in the intima uptake modified lipids while activating and recruiting T cells

Macrophages with consumed lipids become Foam Cells

PDGF, FGF, TGF-alpha growth factors signal the migrating smooth muscle cells to begin proliferation.

Proliferating intimal smooth muscle cells produce of extra cellular matrix, including collagen, to form the plaque

Overtime, a soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers)

The center of the plaque is necrotic, containing lipid, debris, foam cells, and thrombus, surrounded by a zone of inflammatory and smooth muscle cells

28
Q

How does a plaque cause inflammation?

A

Accumulation of cholesterol crystals within macrophages is recognized by the inflammasome, which leads to IL-1 secretion

IL-1 causes recruitment and activation of more macrophages and T cells

Inflammatory cytokines further activate endothelial cells and growth factors stimulate muscle cells to migrate to the intima where they will proliferate to help form the plaque

29
Q

Rank the 5 common sites of atherosclerosis according to frequency and severity

A 
(MOST FREQUENT/MOST SEVERE)
- Abdominal Aorta
- Coronary Arteries
- Popliteal arteries
- Internal Carotid Arteries
- Circle of Willis
(LEAST FREQUENT/ LEAST SEVERE)
30
Q

What si critical stenosis?

A

The point at which an affected vessel lumen shrinks to the point of causing downstream ischemia

  • Occurs at about 70% occluded
31
Q

What are the two phases of plaque formation?

A

Pre-Clinical Phase

  • Normal artery
  • Fatty Streak
  • Fibrofatty Plaque
  • Advanced/Vulnerable Plaque

Clinical Phase

  • Advanced/vulnerable Plaque culminates in one of the three following outocomes:
  • Aneurysm and Rupture
  • Occlusion by Thrombus
  • Critical Stenosis (progressive plaque growth)
32
Q

What is a vulnerable vs a stable plaque?

A

Vulnerable Plaque

  • Thin fibrous caps
  • Large lipid cores
  • Greater inflammation

Stable Plaque

  • Thickened, densely collagenous fibrous caps
  • Minimal inflammation
  • Minimal atheromatous core
33
Q

What three critical changes can occur to a plaque?

A

Rupture/Fissuring
- Exposing highly thrombogenic plaque constituents

Erosion/ulceration
- Exposing the thrombogenic subendothelial basement membrane to the blood

Hemorrhage into the atheroma
- Expanding its volume

34
Q

What is a true aneurysm?

A

An INTACT (but thinned) muscular wall at the site of dilation

Can rupture

35
Q

What is a false aneurysm?

A

AKA Pseudo-aneurysm

DEFECT through the wall of the vessel, or heart, communicating with an extravascular hematoma that freely communicates with the intravascular space

“Pulsating hematoma”

Can rupture

36
Q

What is an arterial dissection?

A

Arises when blood enters a tear/defect in the intima and tunnels between its layers

Dissections are sometimes, but not always, aneurysmal

Can rupture

37
Q

What is vasculitis?

A

Umbrella term describing inflammation of vessels.

Can be infectious or non-infectious (most are non-infectious)

Any type of vessel may be affected. More often arterioles, capillaries, or venules

There are approx. 20 forms of vasculitis

Clinical: depends on vascular bed affected (CNS vs heart vs small bowel)

Consitutional Symptoms: Fever, malaise, arthralgias, myalgias

38
Q

What is Non-infectious vasculitis?

A

Major cause is Local or Systemic Immune response (immune mediated/immune complex vasculitis)

  • Immune complex deposition
  • Antineutrophil Cytoplasmic Antibodies (ANCA)
  • Antineutrophil Cell Antibodies
  • Autoreactive T Cells

Treated with immune suppression

Infections can directly induce noninfectious vasculitis
- Generating immune complexes or triggering cross-reactive immune response

Physical or chemical injury can also cause vasculitis

  • Irradiation
  • Mechanical Trauma
  • Toxins
39
Q

What is immune complex vasculitis?

A

Autoantibody production and formation of immune complexes

Deposition of antigen-antibody complexes in vascular walls

  • Incites an inflammatory reaction within the wall
  • Antigen is often unidentified

May be seen in:

1) Systemic immunologic disease (e.g., Systemic Lupus Erythematosus)

2) Drug Hypersensitivity
- Ex: PCN (penicillin) acts as a hapten binding to serum proteins of vessel wall; streptokinase acts as a foreign protein
- Clinical: mild to fatal skin lesios most common
- Always consider DRUG HYPERSENSITIVITY (stop the drug, resolution of vasculitis)

3) Secondary to exposure to infectious agent
- Ab to microbial constituents from immune complexes that deposit in vascular lesions
- Polyarteritis nodosa: 30% association with HBsAG and Anti-HBsAG (Hep B)

40
Q

What is ANCA?

A

Antineutrophil Cytoplasmic Antibodies

Heterogenous group of antibodies reactant with cytoplasmic enzymes found in neutrophil granules, monocytes, and endothelial cells

ANCA titers generally follow disease severity
- Rise in titers after periods of quiescence is predictive of disease recurrence

ANCAs activate neutrophils, which then release reactive oxygen species

2 types of ANCAs:

  • Anti-proteinase-3 = PR3-ANCA (previously c-ANCA for cytoplasmic)
  • Anti-myeloperoxidase = MPO-ANCA (previously p-ANCA for perinuclear)
41
Q

What are the two types of ANCA?

A

1) Anti-proteinase-3 = PR3-ANCA (previously c-ANCA for cytoplasmic)
- Associated with polyangiitis

2) Anti-myeloperoxidase = MPO-ANCA (previously p-ANCA for perinuclear)
- Induced by Perscribed propylthiouracil
- Associated with microscopic polyangiitis and Churg-Strauss syndrome

Colin CPR II (12 decks)

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