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Patho > Vascular Disease/Atherosclerosis > Flashcards

Vascular Disease/Atherosclerosis Flashcards

1
Q

Arterial Vascular Organization

A

Large Elastic Arteries
Medium Muscular Arteries
Small Arteries

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2
Q

Large Elastic Arteries

A

Aorta, iliac, and Pulmonary arteries
- Elastic fibers throughout the media
- Expands during systole to store energy
- Contract during diastole to propel blood

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3
Q

Medium Muscular Arteries

A
  • Media is primarily muscle cells
  • Elastin limited to internal and external elastic lamina
  • Regional blood flow regulated by expansion/contraction
  • Controlled by autonomic nervous system and pH
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4
Q

Small Arteries (<2mm) and Arterioles (20-100um)

A
  • Media is primarily smooth muscle cell
  • Arterioles control blood flow resistance
  • Resistance ot fluid flow is inversely proprotional to 4th power of diameter ( cutting the diameter in half increase resistance 16-fold)=> small changes in arteriolar lumen size have major effects on bp
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5
Q

Aortic Anatomy

A
  • Aorta thick vessel. Elastic material thoughout the media to store E of systole for use during diastole
  • Oxygen diffuse to inner layer: advetita and outer media fed bby vasa vasorum
  • Endothelium on ALL vessels is nonthrombogenic and resists adhesion of platelets and leukocytes (controls. adherance and passage of materials)
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6
Q

Structure of Medium Artery

A
  • Tunica media; most prominet layer
  • Less elastic material compared to aorta
  • All interior and exterior elastic membrane to be seen clearly
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7
Q

Structure of Small Artery (arteriole)

A
  • Wall bend into surrounding tissue
  • 5 or fewer layers of smooth muscle around small artery
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8
Q

Capillary Vessels

A
  • Have a diameter of 7-8 um
  • Lined with endotherlial cells and partially surrounded by smooth muscle cells called PERICYTES
  • Very slow rate of blood flow and thing walls => this favor rapid exchage of diffusible substance between tissue and blood
  • BP ranges from 35mmHg entering and 10mmHg at the end; Average is 18mmHg
    • Diffusion fo oxygen and nutrient not efficient beyond 100 um so the capillary network is very extensive
  • Capillary density is highest in metabolically active tissue (and brain)
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9
Q

Venous System

A
  • Venules (site of diffusion and leakage) collect blood from capillaries and anastomose to form larger venules and then vains
    – Leakage of fluids (edema) and leukocyte emigration occurs at the level of venules
  • Veins have larger diameters, larger lumena and thinner less distinct walls than comparable arteries reflecting lower pressure.
    – More prone to dilation (pressure is low so they dilate even when bp is low), collapse/compression, and tumor invasion than arteries
    – Have valves that prevent backflow of blood
    Collectively, the venous system has enormous capacitance; 2/3 of blood is in the venous system
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10
Q

Veins

A
  • Medial layer (tunica media) is not prominent nor abundant
  • Vein recoil is not as quick as artery recoil after distention.
  • As veins and arteries travel together. The vein size will look larger because it is streached out
  • Valve regulate the one way flow of blood. (fold of tunica intima -eg., endothelial outcroppings folded back on themselve)
  • For deep veins in the legs, muscle contraction assist the blood flow back to heart
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11
Q

Arteries Vs. Veins

A

Artery: Muscularus is much thicker
Vein: Lumen is thicker, and it got a valve

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12
Q

Lymphatic system

A
  • Thin-walled endothelium channels drain lymph (water, electrolytes, glucose, fat, protein, inflammatory cells) from interstitium of tiissues
  • Lymph channels eventually connect with blood stream via THORACIC DUCT (drained upward, dump w/veinous system at neck)
  • Lymph channel common conduit for movement of malignant cells and infectious microbes
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13
Q

Functions of Lymphatic System

A
  • Retrieve protein that have escaped from capillaries into the interstitial fluid.
    – This allow the interstitial colloid pressure to remain low and limit interstitial edema (third spacing => edema forms)
  • Absorb fat from small intestine. small intestinal lymphatics are called LACTEALS, they absorb ffat and fat souble vitamins and deliver them to the general circulation
  • Immune regulation and surveillance.
    – Due to high permeability (thin walls) of lymphatic capillaries, the bacteria and other microorganism enter lymph system and are transported to lymph nodes, where immune and inflammatory cells may act on them
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14
Q

Where do Lymphatic vessels run

A

They run along side veins and arteries
- Lymphatic vessels have lymph nodes, their walls are thinner than veins , they have valves for unidirectional flow

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15
Q

Lymphatic system (composition)

A

Lymph composed of:
- Water
- Protein that are too large to be reabsorbed (mosltly albumin)
- Foreign substances
Lymphatic veins drain into => right lymphatic duct and thoracic duct. These drain lymph into => the left and righ subclavian veins

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16
Q

Disease of Vasculature

A

Disorders of arteries:
- Artheriosclerosis: most common - can cause coronary artery disease, peripheral vascular disease, strokes, aneurysm (hardening of arteries)
– account for than half the death in US
– Three distinct morphological types
- Hypertension: BP mis-regulation that lead to adverse structural alteration of the arteries (related to artheriosclerosis)
- Aneurysm

Disorders of Arteries and veins:
- Thrombosis: hemodynamic disorder altering vessel structure

Disorders of veins:
- Varicose veins
- Thrombophlebitis (infectious vein that favor arteriosclerosis)/Phlebothrombosis (presence of clot that cause disease)

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17
Q

Arteriosclerosis

A

Atherosclerosis: most common and most IMPORTANT form of arteriosclerosis
Arteriolosclerosis: Affect small arteries and arteriolesl cause ischemia. (small hardening)
- The Two variant (hyaline and hyperplastic arteriolosclerosis) are associated with hypertension.

Monckebery medial calcific sclerosis: Characterized by calcium deposit in media and internal elastic lamina of muscular arteries (radial, ulnar, uterine) of individuals over 50 years.
- It does not reduce on the vessel of lumen

Fibromuscular intimal hyperplasia: non atherosclerotic thickening of smooth muscle cells in arteries that had been injured, inflamed, or immunologically injured

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18
Q

Atherosclerosis

A

Cause of most morbidity and mortality
- Characterized by formation of intimal lesion (atheromas) that narrow lumen and can cause sudden occlusion when rupture
- Atheromas weaken vessel wall, leading to aneurysm formation
- Condition begins early in life as fatty streak regardless of risk factors. Present in all children by 10 but not all will turn into atherosclerosis

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19
Q

Atherosclerotic Plaques:

A

Intimal thickening and lipid accumulation representing disease progression (blood vessels lose laminar flow and become turbalant)

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20
Q

Atherosclerosis: risk factors

A
  • Multiple constitution: genetics, gender, and age
  • Modifiable: Hypertension, hemodynamic disturbances, hypercholesterolemia, smoking, diabetes omega-3 fatty acids

These interact in multiplicative manner to enhance the effect of each

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21
Q

Atherosclerosis: Vessels Involved

A

Infra-renal abdominal aorta
Coronary arteries
Popliteal arteries
Cicle of Willis in brain

Strongly associated with regions of vascular turbulence, particularly at orgin or branches of vessels (slow progression)

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22
Q

Pathogenesis of Atherosclerosis

A

Response to injury hypothesis is most widely held. It view atherosclerosis as chronic inflammatory response of the artery wall to endothelial injury
1) Endothelial injury, resulting from hemodynamic disturbance or hypercholesterolemia, leading to increased permeability and leukocyte adheasion
2) Accumulation of lipoproteins (primarily LDL and Cholesterol) in sub-intima
3) Monocyte infilreation to endothelium, migration to intima, differentiation to macrophages (in tissues) and foam cells
4) Lipid accumulation within macrophages, => response by releasing inflammatory cytokines
5) Smooth muscle cell recruitment and proliferation and production of extracellular matrix
6) Plaque may weaken vessel wall, narrow vessel lumen, clacify, form thrombi or (worst case) rupture causing acute occlusion

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23
Q

Atheroma

A

Once formed is irreversible

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24
Q

Endothelial Injury (basemnet embrance becomes expose)

A
  • Injurous agents will be released => monocytes adhere => Monocytes pass intima (macrophages ingest lipids)
  • Altered surface => (Monocytes adhere) + Platelets adhere => growth factor relased => smooth muscle proliferation + connective tissue deposition + lipid synthesis
  • Increased permeability => Increased libid in intima
    There last step in each will all come together and FORM ATHEROMA
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25
Q

What is the first step in atherogenesis

A

Formation of fatty streaks (pale yellow streaks that run along the intima from accumulation of macrophages that store fat in their cytoplasm)
- Do not develop into plaques in thoracic aorta

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26
Q

Atherosclerosis Timeline

A

Foam Cells => Fatty Streaks => Intermediate Lesion => Atheroma => Fibrous Plaques => Complicated Lesion/Rupture (irreversible)

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27
Q

Vessel Wall Atherosclerosis Complication

A

The damage happen from
- Calcification (complex lesion)
- Hemorrhage
- Tunica Media Destruction (thinning)
- Ulceration

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28
Q

Atherosclerosis; Endothelial Surface

A

1) Damage to cells
2) Permeability to LDL (cholesterol- VLDL traffic lipid into cell)
3) Adherence and entry of monocytes into intima

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29
Q

Atherosclerosis;Intima

A

1) Activation of monocytes
2) Migration of smooth muscle cells into intima
3) Smooth muscle cell mitosis
4) Synthesis and deposition of extracellular matrix

30
Q

Atherosclerosis; Fibrous Cap

A

On surface of cell
- dedifferentiated smooth muscle cells, lymphocytes, collagen, etc.

31
Q

Atherosclerosis; Necrotic center

A

Inside cell
- Cell debris, cholesterol crystals, foam cells, calcium

32
Q

Fomation of fatty streak and stages

A

Check screen shots
- Norma artery => Fibrofatty Plaque (A lesion prone area) => Advanced plaque (CEll death/degeneration) => got three paths from here
1) Aneurysm and Rupture: Reasons - Mural thrombosis, Embolization, Wall Weakening
2) Occlusion by Thrombus: Reasons - Plaque Rupture, Plaque Errosion, Plaque hemorrhage, Mural thrombosis, Embolization
3) Critical Senosis: Reasons - Progressive plaque growth

33
Q

Management of Atherosclerosis

A
  • Surgical Intervention: Stents, By-pass
  • Pharmacological Intervention: Cholesterol management, Statins, Specific anti-cholesterol and LDL-lowering agents, anti hypertensive agents, diabetes drugs, and CNS drugs
  • Behavioral Intervention (most valuable IF compliance): Regular exercise, Cessation of smoking, dietary or pharmacologic control of serum lipids
    – Cholesterol < 200 mg/dL
    – LDL < 130 mg/dL
    – HDL > 40mg/dL, optimally 45-70mg/dL
    Every diabetic develop atherosclerosis
34
Q

Statins

A

Act both on HMG-CoA reductase and to stabilize the atheroma cap
- Decrease likely hood of thrombosis

35
Q

Iron Theory for Atherosclerosis

A

Acummulation of iron => fenton RxR reactive oxygen => Women become anemic after menopause
Iron that acummulate normally during normal life in male prevent fenton RxR

36
Q

Arteriosclerosis (hypertension condition)

A
  • Affect small arteries (arterioles)
  • Lumen narrowed
  • Wall looks uniform, glasslike
  • Compromised ability to dilate
  • Cause downstream ischemia
  • Can be a cause of secondary hypertension (by activating the renin-angiotensin system)
    – by inhibiting the blood flow to the kidney => it think it’s in shock => activates the renin-angiotensin system)
37
Q

What Happens in Benign Hypertension?

A

Hyaline (pink material) accumulate in the walls of arterioles => glass-like appearance, thickened walls, and narrowed lumen
Arteriolosclerosis often involve the kidney (impais blood flow and GFR) => Lowered GFR is sensed as low bp => renin secretion and elevated systemicBP

38
Q

Monckeberg’s Medial Calcific sclerosis

Age, Arteries affected, Characterization, Lumen, Causes?

A
  • Over 50 in age
  • Affect MEDIUM SIZED ARTERIES, mostly neck, pelvis, and limbs
  • Characterized by FOCAL RADIOLOGIC CALACIFICATION in Tunica Media
  • Muscle tissue degenerates
  • The lumen is NOT NARROWED
  • Does not have clinical manifestation (usually)
  • Causes Pulselessness
39
Q

Aneurysms and Dissections

what is it?

A

Dilation of Blood Vessels
- A true aneurysm involve all 3 layers of vessel
- A false aneurysm result from the wall defect => extravascular hematoma that communicates with extravascular space

40
Q

Aneurysms and Dissections

Classification

A

Classification: by shape
- Saccular (5-20 cm); round
- Fusiform (up to 20 cm)

41
Q

Aneurysms and Dissections

Caused by and Most important predisposing

A
  • Inadequate/defective connective tissue synthesis
  • Excessive degradation of connective tissues
  • Loss of smooth muscle cells

Most important predisposing:
- Atherosclerosis or hypertension
- May arise from wall weakened by infections (mycotic aneurysm)
- Congenital defects
- Trauma

42
Q

Rupture of what is fatal?

Aneurysm

A

Rupture of abdominal or cerebral aneurysm is fatal (must be treated immediately)

43
Q

Abdominal Aortic Aneurysm

AAA

A
  • Result from atherosclerosis (most common cause for it and iliac arteries)
  • Most common in males and smoker over 50
  • Result from degradation of extracellular matrix by proteolytic enzymes from inflammatory cells and/or defects of nutrient supply => ischemia and loss of smooth muscle cells of media
44
Q

Abdominal Aortic Aneurysm

Consequences

A
  • Obstruction
  • Embolism
  • Compression of adjacent structures
  • Pulsatile abdomical mass and rupture
45
Q

Abdominal Aortic Aneurysm

Rupture and treatment

A
  • <4 cm almost never rupture
  • 4-5 cm rate is 1%/year
  • 5-6 cm is 11%/year
  • > 6 cm is 25%/year

Treatment: surgical
- Mortality rate is 5%;
- Emergencey surgery mortality is 50%

46
Q

Atherosclerotic Aortic Aneuysm

A large bulge appears

A

Above The Aortic Bifurcation
- Prone to rupture when reach 6-7 cm in size (rupture = death)
- Felt on physical examination as pulsatile mass in abdomen
- Most located below the renal arteries
– surgical resection can be performed with placement of dacron graft

47
Q

Atherosclerosis

responsible for which aneurysms?

A

Can be responsible for abdominal aortic aneurysms but not THORACIC aneurysm
- Above bifuracation to common iliacs (location)

48
Q

Aortic Dissection (thoracic or abdominal)

A

Occurs when blood separates laminar planes of media to form a channel in the aortic walls
- Major risk is hypertension
– Also associated with heritable connective tissue disease (eg, Marfan’s syndrome, a defect in matrix molecule fibrillin)

Most common in men 40-60 years with a history of hypertension (90%)
Most occur in ascending aorta within 10 cm of aortic valve

49
Q

Aortic Dissection

Classification, symptoms and prognosis

A

Classified into 2 types:
- Proximal Lesions (Type A; DeBakey I or II)
- Distal Lesion (type B or DeBakey type III)

Present with: Acute onset of pain ( excruciating) beginning in chest, radiating to back between scapula and moving down as dissection progress

Prognosis for
- Type A depend on antihypertension treatment and surgery- usually 65-85% survival
- Tpe B treated conservatively
Have to be surgically removed

49
Q

Aortic Dissection

Classification, symptoms and prognosis

A

Classified into 2 types:
- Proximal Lesions (Type A; DeBakey I or II)
- Distal Lesion (type B or DeBakey type III)

Present with: Acute onset of pain ( excruciating) beginning in chest, radiating to back between scapula and moving down as dissection progress

Prognosis for
- Type A depend on antihypertension treatment and surgery- usually 65-85% survival
- Tpe B treated conservatively
Have to be surgically removed

50
Q

Hypertensive Vascular Disease

A
  • Essential (benign) hypertension: elevated BP from the interplay of environmental factors and genetic polymorphisms
    –Sustained diastolic pressure of > 90mmHg or sustainted systolic pressure of >140 mmHg are cutoff used in clinical practice (by these criteria 25% of US population are hypertensive)
    –If untreated 50% of patient will die of CHD and another 30% of stroke.
  • Malignant hypertension; rare (5% of hypertensive patients) manifest sever elevation (>200/140).
    – Will die within 1-2 years without treatment

95% of cases are idopathic (essential); most of the remainder are secondary to renal disease or other known known causes and termed “secondary hypertensive”

51
Q

Mechanism of Hypertensive Vascular Disease

A
  • Reduced renal sodium excretion
  • Increased vascular resistance from prolonged vasoconstriction
  • Genetic factors: polymorphisms of renin angiotensin system
  • Environmental factors: stress, obesity, smoking, physical inactivity, increased salt consumption, and too much TV
52
Q

Theories of Hypertension pathogenesis

A

When CV system is affected so is the kidneys
1) Increased blood volume
2) An increased in activity of Sympathetic NS
3) Increased activity of the renin-angiotensin-adosterone system
4) Water and sodium retention by kidney
5) Hormonal inhibition of sodium-potassium transport across cell wall in kidney and blood vessels

Hypotheses suggest
- Intervention for 1, & 4
- Diuretics for 2
- Inhibitors of sympathetic nervous system for 2 and 3
- Vasodilators

53
Q

Renal Artery Stenosis

What is it?

A

Narrowing of arteries that carry blood to one or both kidneys. Seen in older people with atherosclerosis most often
- Can wosen over time leading to hypertension and kidney damage (or kidney failure)
- When body sense less blood reaching kidney, it misinterpret that as body having low BP and release hormones from kidney that lead to secondary hypertension

54
Q

Renal Artery Stenosis

Results and Causes

A

Result in
- Arteriolosclerosis
- Thickening of arteriole walls
- Associated with downstream ischemia

Causes:
- 90% of renal artery stenosis is caused by atherosclerosis

55
Q

Renin-Angiotensin-Aldosterone System

A

Decreased Blood Flow => Stimulate Renin Release => Renin Converts Angiotensinogen to Angiotensin I => Vascular Endothelial Cell (ACE) convert Angiotensin I to Angiotensin II
- This Causes
1) Constriction; rise in BP
2) Increased permeability of endothelial cells (bad because lipids and monocytes can slip between cells)
3) Increased signalling to SMC (smooth muscle cells) to proliferate and hypertropy
4) Increased release of aldosterone

This stimulate the reabsorption of NA+, increasing plasma volume => BP rising

56
Q

Clinical Aspects of Hypertension

A

Essential hypertension appear over a period of years but the effect accumulate early
- Accelerate formation of atherosclerosis but atherosclerosis rarly cause hypertension (exception in stenosis of renal artery: called GOLDBLATT KIDNEY)
- Kidney vessels are a major site of vascular injury
– Arterioles show homogeneous hyaline thickening of walls from pressure transdation of plasma proteins
– Luminal narrowing
- Hyperplastic arteriolosclerosis is more severe and result in concentric laminated thickening of walls (onion skin change, doesn’t contract and expand)
- Common cause of renal failure, Contributes to MI, stroke, and generally bad health

57
Q

Treatment for hypertension

A

Life style changes
Stop smoking
Reduce salt intake
Reduce stress
Medication
Diuretics (decreased fluid volume)
Vasodilators (decrease total peripheral resistance - reflex stimulation of sympathetic outflow)
Sympathetic Inhibitors (esp. Beta blockers)
- Reduced cardiac stimulation, low CO
- Reduced renin levels that result from vasodilator’s increase in sympathetic outflow
- Reduced Na+ excreted, so increased plasma vol-need diuretic as part of therapy

ACE inhibitors in specific population; diabetic, MI patients

58
Q

Vein Disorders

A
  • Varicose Veins (common dilation of superficial veins due to posture-in legs)
  • Thrombophlebitis (infection of varicose veins from clots)
59
Q

Varicose Veins

A

Twisted Superficial Veins; Causes
- lack of muscle support
- From increased venous pressure (standing, pregnancy, etc.)
- Valve function is compromised

Thrombosis can result but generally the condition is not a step toward thromboemblism

60
Q

Thrombophlebitis

Symptoms, and location

A

Symptoms include
- Warmth
- Tenderness
- pain in affected area with redness and swelling
- Edema in ankle and foot
- Cord like veins
– Venous inflammation; caused by local infection

Can be Localized in superficial veins or Localized in Deep Leg Vein

61
Q

Localized in superficial veins

Thrombophlebitis

A
  • Thrombi that form in superficial vein (superficial phlebitis), they are less serious than DVT
  • When affected, a red, hard, and tender cord may be felt under the surface of skin
62
Q

Localized in Deep Leg Vein

Thrombophlebitis

A
  • Leg may be swollen
  • Tender and painful (esp. when standing or walking)
  • May be a fever but most people with DVT have no symptoms
63
Q

Thrombophlebitis

Causes, Diagnosis, and Treatment

A

Can be caused by an increased tendency for blood clotting, and reduced speed of blood in the veins (like from immobile for long periods)

Diagnosis:
- Dopplerr ultrasound, Arteriography, Clotting test

Treatment:
- Raise the leg to decrease swelling
- LMW heparin or warfarin therapy
- Surgery
- Drain excess fluid caused by clot

64
Q

Thrombophlebitis (inflammation of the walls of vein)

Cases and symptoms

A

90% of cases result from deep vain thrombosis (DVT)
- They are mostly silent, especially in bed ridden patients
- Circulation/fragmentation of DVT may result in pulmonary embolus
- Immobilization resuling into venous stasis ( a condition where veins are having a hard time pushing blood back to heart) is a major risk factor
- Symptoms for leg thrombi include: distal edema, cyanosis, redness, swelling, pain
– pain may be elicited by squeezing calf muscles or forcing dorsiflexion of the foot (Homan sign)

65
Q

DVT

A

Thrombus form in deep vain and is a significant risk for thromboembolism becasue muscle contraction can dilodge a thrombus
- Commonly happen in the deep vain of calf
- Can spread up to deep vain in thigh
- Rarey develop in other deep veins like arms

66
Q

How to diagnosis DVT

A
  • Ultrasound or venography with a contrast agen can locate a thrombus
  • Blood test to check for D-DIMER LEVELS: fibrin degradation product
    – Not conclusive as it can be elevated in other conditions too
    – Only suggest that a thrombus has recently been acted upon via fibrinolysis
67
Q

Complication

for DVT and Superficial

A
  • If present in superficial veins, serious complications are rare
  • If occur in deep vein, serious complication risk is great
    – Pulmonary embolism (life theratening)
    – Damage to vavle in leg vein
    – Permanent vein obstruction if many ep of deep vein thrombosis have occure
68
Q

Symptoms of Pulmonary Embolism

A
  • Sudden shortness of breath (sign of airway problem)
  • Chest pain that mimic a heart attack (may be sharp and stabbing or aching and dull, pain worsens with exertion but does not go away when at rest)
  • Cough that produce bloody or blood-streaked sputum
  • Excessive sweating
  • Rapid heartbeat (tachycardia)
  • Lightheadedness or fainting
69
Q

Diagnosis for Pulmonary Embolism

A

Diagnosis is difficult as symptoms are nonspecific and may mimic other diseases
- Pulmonary angiography is the golden standard test for diagnosis
– other test include oximery, arterial blood gas analysis, chest x-ray, and ultraongraphy

70
Q

Treatment for Pulmonary Embolism

A

Treatment include anticoagulant such as heparin and warfarin (coumadin)
- About 10%-15% of patient with pulmonary embolism die

Patho (17 decks)

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