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General Pathology > Vascular Disease > Flashcards

Vascular Disease Flashcards

1
Q

What disease causes more morbidity and mortality than any other group of diseases?

A

Vascular disease

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2
Q

List the two major mechanisms of vascular disease

A
  1. Narrowing/Obstruction
    -Acutely (thrombosis/embolism)
    -Progressively (atherosclerosis)
  2. Weakening - causes dilation and/or rupture
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3
Q

Describe the composition of vessels

A

-Endothelial cells (EC)
-Smooth muscle cells (SMC)
-ECM - elastin, collagen, glycosaminoglycans

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4
Q

What are the layers of the vessel wall?

A
  1. Intima - single layer of EC cells
  2. Internal elastic lamina
  3. Media - SMC
  4. External elastic lamina
  5. Adventitia - contains vessels (vasa vasorum) providing nutrients for the vessel itself
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5
Q

List the different types of arteries

A
  1. Large (elastic)
    -Aorta, subclavian, common carotid, iliac, pulmonary
  2. Medium (muscular)
    -Coronary, renal
  3. Small (<2mm) and arterioles
    -Arterioles are the main control point for regulation of resistance to blood flow (regulates bp)
  4. Capillaries - no media, diffusion of nutrients
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6
Q

List the different types of veins

A
  1. Post-capillary venules
    -site of vascular leakage in inflammation
  2. Collecting venules
  3. Larger veins
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7
Q

How do veins compare to arteries?

A

Veins are…
-Larger diameter, larger lumina, thinner/less organized walls
-More prone to dilation/compression and penetration by tumors or inflammation (b/c larger diameter and thinner walls)

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8
Q

Describe the features of lymphatics

A

Thin-walled, endothelium-lined channels that drain lymph (water, electrolytes, glucose, fat, proteins and inflamnatory cells) from interstitum back to heart and to lymph nodes

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9
Q

What is the purpose of lymphatics?

A

-Maintain blood volume
-Facilitate antigen presentation/immune activation

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10
Q

List the functions of the endothelium (6)

A
  1. Lines vascular system, maintains hemostasis
  2. Diffusion of small molecules (nutrients, electrolytes and O2) but not larger molecules (proteins)
  3. Balances coagulation (vWF, tissue factor, plasminogen activator inhibitor) vs. anticoagulation (prostacyclin, thrombomodulin, heparin-like molecules, plasminogen activator)
  4. Balances vasoconstriction (endothelin, ACE) vs. vasodilation (NO, prostacylin)
  5. Regulates inflammation (i.e. IL-1, IL-6, chemokines)
  6. Regulates growth- stimulates (e.g. PDGF, CSF, FGF) vs. inhibits (TGF-beta)
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11
Q

What happens with endothelial activation?

A
  1. Shape changes
  2. Express adhesion molecules and produce:
    -cytokines
    -chemokines
    -growth factors
    -procoagulant and anti-coagulant factors
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12
Q

T/F: Endothelial activation can be rapid (minutes), reversible with no new protein synthesis, or take days to develop due to gene/protein expression changes

A

TRUE

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13
Q

Why does the endothelium get activated?

A

Response to stimuli (with intent to respond appropriately):
-Bacterial products
-Inflammatory cytokines
-Hemodynamic stresses
-Lipid products (in atherosclerosis)
-Advanced glycation end products (in diabetes)

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14
Q

High levels of stimuli for sustained periods can cause endothelial dysfunction with….

A

-Endothelium -dependent impaired vasodilation
-Hypercoagulability
-Increased ROS (causing cell injury and cell death)

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15
Q

What does endothelial dysfunction increase the risk of?

A

Thrombosis, promotes atherosclerosis, hypertension and diabetes

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16
Q

What are the functions of the Media?

A
  1. Elastic recoil in large arteries allows pulsatile flow
  2. Smooth muscle in arterioles, small and medium arteries regulates resistance
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17
Q

When any insult or dysfunction occurs in the media, _________ are released leading to:

A

Growth factors are released leading to:
Smooth muscle cell (SMC) migration into the intima and proliferation leading to intimal thickening
-Aids in repair (good)
-Involved in atherosclerosis (bad)

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18
Q

SMCs that migrate into the intima don’t have contractile properties but they can _______

A

divide

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19
Q

In the media, with persistent insult –> excessive intimal thickening –> _______

A

stenosis

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20
Q

How do you calculate BP?

A

BP = cardiac output x peripheral resistance (how dilated the vessel is)

**BP maintenance required for adequate organ perfusion

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21
Q

When BP or blood Na+ decreases, _____ is secreted. What is the result of this?

A

Renin
-Increased vascular tone and increased aldosterone secretion, both of which increases BP

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22
Q

What is Stage 1 hypertension?

A

> 130/80 mm Hg

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23
Q

What is Stage 2 hypertension?

A

> 140/90 mm Hg

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24
Q

What is the pathophysiology of hypertension?

A

Increased cardiac output and/or peripheral resistance in small vessels causes hypertension

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25
Q

What is the cause of 90-95% of all hypertension cases?

A

No known cause “idiopathic”

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26
Q

Describe the Pathogenesis Theory of essential hypertension (primary)

A

-Multiple genetic and environmental factors which increase blood volume (due to reduced renal sodium excretion) and/or peripheral resistance (vessel wall tone/structure)
-Environmental factors - stress, obesity, smoking, lack of exercise, heavy salt intake

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27
Q

List the secondary causes of hypertension. Which of these is the biggest contributor?

A

-Kidney disease*
-Pheochromocytoma
-Cushing syndrome
-Conn syndrome
-Hyperthyroidism
-Pre-eclampsia

*Kidney disease is the biggest contributor

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28
Q

How does kidney disease contribute to hypertension

A

Producing renin –> angiotensin I –> angiotensin II –> Na reabsorption and vasoconstriction

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29
Q

How does Pheochromocytoma contribute to hypertension

A

Adrenal tumor making catecholamines

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30
Q

How does Cushing syndrome contribute to hypertension

A

Adrenal cortex tumor that makes corticosteroid

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31
Q

How does Conn syndrome contribute to hypertension

A

Adrenal cortex tumor that makes aldosterone

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32
Q

How does Hyperthyroidism contribute to hypertension

A

Produces thyroxin that raises BMR

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33
Q

How does Pre-eclampsia contribute to hypertension

A

Endothelial dysfunction during pregnancy leading to vasoconstriction

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34
Q

What are the consequences of Hypertension?

A
  1. Thickening of small arteries and arterioles with luminal narrowing (arteriolosclerosis) –> nephrosclerosis (scar tissue in the kidney as a result of chronic low blood flow)(an ischemic kidney disease)
  2. Accelerated atherosclerosis
  3. Weakens vessel wall leading to
    -dissecting aneurysms
    -cerebral hemorrhage
  4. Left ventricular overload –> hypertrophy –> failure
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35
Q

What is the normal vascular response to injury? What happens if persistent and recurrent injury occurs?

A

Normal:
-Vascular injury –> endothelial loss or endothelial cell dysfunction –> smooth muscle cell growth and matrix synthesis –> intimal thickening

Persistent and recurring injury:
–> further thickening results leading stenosis (narrowing) - now pathologic

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36
Q

Definition of Arteriosclerosis

A

“Hardening of the arteries” associated with intimal thickening, decreased luminal size and loss of elasticity

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37
Q

List the major types of arteriosclerosis

A
  1. Arteriolosclerosis
    -vessel wall thickening
    -associated with hypertension and diabetes
  2. Atherosclerosis
    -intimal thickening of large and medium arteries
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38
Q

In atherosclerosis, ________ obstructs blood flow

A

Intimal plaque
-Consists of necrotic lipid core (mostly cholesterol) with a fibromuscular cap; often undergoes dystrophic calcification

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39
Q

What type of arteries does atherosclerosis affect? Where in the artery is usually affected?

A

Large and medium sized arteries, especially at bifurcations
-Abdominal aorta, coronary, popliteal, internal carotid are commonly affected

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40
Q

List the modifiable major risk factors of atherosclerosis

A

-Hypertension
-Hyperlipidemia (specifically hypercholesterolemia)
-Smoking
-Diabetes

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41
Q

List the non-modifiable major risk factors of atherosclerosis

A

-Age (# and severity of lesions increases with age)
-Gender: increased risk in males and postmenopausal females; estrogen is protective
-Genetics: multifactorial, but family history is strongest independent risk factor

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42
Q

Give an overview of Hyperlipidemia

A

-Lipids are bound to apoproteins in blood
-Defective apoproteins or lipid receptors can increase LDL and decrease HDL
-Prefer total cholesterol to be <200 mg/dL

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43
Q

Describe HDL (high density lipoprotein)

A

-“good cholesterol”
-Takes cholesterol from tissues/atheromas and transports to liver for excretion in bile

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44
Q

Describe LDL (low density lipoprotein)

A

-“bad cholesterol”
-Delivers cholesterol to peripheral tissues

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45
Q

List the minor risk factors for atherosclerosis

A

-C-reactive protein
-Hyperhomocysteinemia
-Metabolic syndrome
-Lack of exercise/stress
-Periodontal disease

46
Q

How does C-reactive protein contribute to atherosclerosis

A

Cheap, sensitive, systemic marker of inflammation. Predicts risk of MI, stroke, peripheral arterial disease

47
Q

How does Hyperhomocysteinemia contribute to atherosclerosis

A

Impairs endothelial function. Caused by low folate and vitamin B intake

48
Q

How does Metabolic syndrome contribute to atherosclerosis

A

-Hypertension
-High blood sugar
-Central obesity (leading to insulin resistance)
-Hyperlipidemia/high cholesterol

Sequellae: increased risk for heart disease, stroke, diabetes, hypercoagulabitlity and pro-inflammatory state

49
Q

How does periodontal diease contribute to atherosclerosis

A

Modest, consistent, increased risk (RR 1.20 - relative risk higher than 1 (1 would be no risk))

50
Q

List the modifiable risk factors that can prevent atherosclerosis

A

-Control hypertension
-Lower total and LDL blood cholesterol
-Increase HDL levels (diet, statin drugs)
-Stop smoking
-Weight loss
-Exercise/reduce stress

Also, prevent 2nd heart attack/stroke with medications (aspirin, statins, beta blockers) and surgery

51
Q

Describe the pathogenesis of atherosclerosis

A

-Damage to endothelium allows lipids to leak into the intima
-Lipids are oxidized then consumed by macrophages resulting in foam cells
-Inflammation and healing leads to deposition of extracellular matrix and proliferation of smooth muscle

52
Q

Atherosclerosis is a chronic, progressive condition which goes through morphologic stages. Describe these stages

A

-Flat yellow lesions (fatty streaks) made of cholesterol and within lipid-laden macrophages; arise early in adolescence
-Smooth muscle proliferation causing a thickened plaque that narrows the vessel lumen
-Calcification and ulceration with possible complications

53
Q

List the possible sequelae of atherosclerosis

A
  1. Stenosis/obstruction –> ischemia
    -peripheral vascular disease (lower extremities - ex. popliteal, legs - claudication)
    -angina (coronary arteries)
    -ischemic bowel disease (mesenteric arteries)
  2. Plaque rupture/ulceration –> thrombosis causing myocardial infarction (coronary arteries) and stroke (cerebral artery) (clot blocks the remaining opening of the vessel)
  3. Break off –> atheroembolism (traveling piece of plaque which can go block something else)
  4. Weaken medial wall –> aneurysm (ex. abdominal aorta). Can rupture or develop a mural thrombus which can embolize
54
Q

The first step in the pathogenesis of atherosclerosis is endothelial cell injury/dysfunction. What causes this?

A
  1. Hypertension causing turbulent blood flow
  2. Hyperlipidemia/hypercholesterolemia: cholesterol increases ROS which:
    -increase shear stress on endothelial cells (EC)
    -oxidize lipoproteins; oxidized lipoproteins are toxic to EC
  3. Smoking
  4. Inflammatory/immune reactions
55
Q

For atherosclerosis, list the response to injury hypothesis: sequence of events

A
  1. Chronic endothelial injury –>
  2. Endothelial cell dysfunction (permeable to LDL –> adhesion to monocytes) –>
  3. Accumulation of lipids and MACs in vessel wall
  4. Lipid is oxidized and phagocytosed by MACs creating foam cells (visible flat “fatty streaks”) –>
  5. Factor release (from MACs, EC, T cells) recruits SMCs which proliferate and make ECM
  6. Over time, a fibrous cap develops on the surface with a lipid core (mature atheroma)
  7. Inflammation can make the atheroma unstable. With disruption –> thrombosis
56
Q

______ are dynamic lesions of lipid/cholesterol, dysfunction ECs, proliferating SMCs, ECM, MACs and lymphocytes

A

Atheromas

57
Q

What is the pathogenesis of atheroma?

A

Chronic inflammatory response to endothelial injury, lipid accumulation/oxidation and increasing risk for thrombosis

58
Q

Describe Aneurysm

A

Localized dilation of a blood vessel or the heart chamber

59
Q

What is a false or pseudoaneurysm?

A

Breach in vessel wall with hematoma communication with lumen

60
Q

List the types of Aneurysms

A

-Atherosclerotic (aortic aneurysm), most common
-Syphilitic
-Berry
-Ventricular

61
Q

Describe aortic aneurysm

A
  1. Atherosclerosis leads to destruction of intima and media (inadequate nutrient/waste exchange)
  2. Often in abdominal aorta (i.e. abdominal aortic aneurysm) below renals and above iliacs
    -Pulsatile, abdominal mass
    -Timely surgery to prevent death b/c it can rupture
62
Q

Describe berry aneurysm

A

-Small, spherical dilations of the cerebral vessels (circle of Willis)
-Caused by congenitally weak vessel wall, or atherosclerosis with hypertension

63
Q

Describe ventricular aneurysm

A

Left ventricular wall expansion and thinning that pulsates

64
Q

What causes ventricular aneurysm?

A

Large myocardial infarct

65
Q

What can happen with a ventricular aneurysm?

A

May rupture or develop a mural thrombus that may embolize

66
Q

What causes aortic dissection?

A

Hypertension or cystic medial degeneration, typified by Marfan sx (problem with fibrilin - can’t stretch)

67
Q

Aortic dissection may or may not have….

A

aortic dilation (aneurysm)

68
Q

What happens with an aortic dissection?

A

Blood enters a tear in the intima in the aortic arch and dissects through the media causing intense chest pain
-rupture through adventitia is fatal

69
Q

What is vasculitis and what are the two different types?

A

Inflammation of the vessel walls
-Infectious
-Non-infectious

70
Q

What are the constitutional symptoms of vasculitis?

A

Fever, myalgia, arthralgia, malaise

71
Q

Describe infectious vaculitis

A

Direct invasion of organisms (ex. Mucor, Aspergillus) into vessels can weaken vessel walls (mycotic aneurysm) or cause thrombosis and infarction

72
Q

Describe non-infectious vasculitis

A

-Immune-mediated
- ~20 types

73
Q

List the primary mechanisms of non-infectious vasculitis

A
  1. Immune complex deposition
    -drug hypersensitivity (medication can induce this autoimmune response)
  2. Antineutrophil cytoplasmic antibodies (ANCAs)
    -Anti-proteinase-3 (PR3-ANCA) targets azurophilic granules; Anti-myeloperoxidase (MPO-ANCA) targets myeloperoxidase
    -Directly injures endothelium and activate neutrophils
  3. Anti-endothelial cell antibodies
74
Q

What are the types of non-infectious vasculitis?

A

-Giant cell arteritis
-Granulomatosis with polyangiitis

75
Q

What is the pathogenesis of Giant Cell (Temporal) Arteritis

A

Immune T cell reaction against a constituent of a vessel wall

76
Q

Describe Giant Cell (Temporal) Arteritis

A

-Granulomatous inflammation of the temporal and nearby arteries (including ophthalmic and lingual artery) causing focal, nodular occlusive lesions
-Can be palpated along the temporal region
-Common arteritis in pts >50yrs

77
Q

What can giant cell (temporal) arteritis cause?

A

Severe headache, blindness. In rare causes, lingual infarction

78
Q

Giant cell (temporal) arteritis responds to _______

A

steroids

79
Q

Granulomatosis with Polyangiitis (PGA) is formerly called…..

A

Wegener granulomatosis

80
Q

Describe the clinical presentations of Granulomatosis with Polyangiitis (PGA)

A

-Targets respiratory tract (upper and/or lower) and kidney glomeruli
-Also involves palate (necrosis of midface) and gingiva (strawberry gingivitis)
-80% die within a year w/o treatment

81
Q

What is the pathogenesis of Granulomatosis with Polyangiitis (GPA)

A

Cell-mediated hypersensitivity to an inhaled antigen or infectious agent

82
Q

What does Granulomatosis with Polyangiitis (GPA) cause?

A

Production of anti-proteinase-3 anti-neutrophil antibodies (PR3-ANCA) that directly activates neutrophils

83
Q

What does Granulomatosis with Polyangiitis (GPA) result in?

A

A necrotizing granulomatous vasculitis

84
Q

Describe the Raynaud Phenomenon

A

Exaggerated, paroxysmal (happening repeatedly), vasoconstriction of arteries in the fingers or toes (sometimes ears, nose) when exposed to cold or emotion

85
Q

What would you see visually with the Raynaud Phenomenon?

A

-Proximal fingers are red from vasodilation
-Midfinger is white from vasoconstriction
-Distal finger is blue from stasis/cyanosis

86
Q

Is the Raynaud Phenomenon associated with another disease?

A

Primary cases are mostly (90%) isolated; 10% have another associated (secondary) disease (ex. scleroderma, SLE, Buerger disease, atherosclerosis)

87
Q

Describe Varicose veins

A

Superficial saphenous veins become dilated and tortuous due to increased pressure from gravity over many years

88
Q

Who are Varicose veins most commonly seen in?

A

Seen mostly in elderly people who stand or sit a lot and have weak muscular support or are obese

89
Q

What are the consequences of varicose veins?

A

-Bleeding
-Pedal edema, pain and thrombosis but do not lead to thromboemboli

90
Q

List other types of varicosities

A

-Hemorrhoids
-Esophageal varices
-Lingual varcies

91
Q

Hemmorhoidal veins do not have _______

A

valves

92
Q

When are hemorrhoids usually seen?

A

Often noted with pregnancy, cirrhosis, and constipation

93
Q

Where are lingual varices seen?

A

Under tongue

94
Q

Describe esophageal varices

A

-Liver cirrhosis –> portal hypertension and increased blood flow into gastroesophageal veins
-Rupture leads to massive GI hemorrhage

95
Q

Thrombophlebitis is also known as ______

A

phlebothrombosis; both mean venous thrombosis with inflammation

96
Q

90% of thrombophlebitis occur in deep leg veins (deep vein thrombosis - DVT) secondary to:

A

-Congestive heart failure (blood pools in extremities)
-Immobilization
-Surgery, especially abdominal
-Trauma
-Pregnancy
-Hypercoagulable state (ex. genetic sx, neoplasia)

97
Q

Describe the Homan sign in regards to thrombophlebitis

A

Pain in calf during squeezing or dorsiflexion of foot - sign of DVT

98
Q

Describe the Trousseau sign in regards to thrombophlebitis

A

Migratory thrombophlebitis (form, resolve and reappear elsewhere) associated with malignancy-induced hypercoagulability (especially pancreatic and lung carcinomas)

99
Q

What is the consequence of thrombophlebitis?

A

Those above knee (popliteal, femoral, iliac) tend to propagate and embolize

100
Q

What is the tx from thrombophlebitis?

A

Coumadin, pressure stocking, elevate foot during sleep, standing and lying down is OK; sitting is bad

101
Q

List the two types of vascular growths and their subtypes

A
  1. Reactive growths
    -pyogenic granuloma
  2. Vascular ectasias
    -nevus flammeus
    -spider telangiectasia
    -hereditary hemorrhagic telangiectasia
102
Q

What is pyogenic granuloma?

A

Tumor-like growth but not a true neoplasm, not bacterial infection and not granulomatous inflammation. Total misnomer!

103
Q

What is the histology of pyogenic granuloma?

A

-Proliferating capillaries and fibroblasts with edema (looks like granulation tissue)
-Rapidly growing, often ulcerated and red, soft nodule that bleeds easily

104
Q

Where do pyogenic granulomas occur? What causes them? How are they treated?

A

Location:
-Can occur anywhere but often on skin or gingiva/oral mucosa and can be associated with pregnancy (“pregnancy tumor”)

Cause:
-Trauma or other local irritants

Tx:
-Surgical excision is curative

105
Q

Describe vascular ectasias

A

-Not true neoplasms; local dilation of preexisting vessels
-Telangiectasia = exaggeration of a preformed vessel

106
Q

What disorders are associated with Vascular Ectasias?

A

-Nevus Flammeus
-Spider Telangiectasia
-Hereditary Hemorrhagic Telangiectasia (HHT)

107
Q

Which is the most common ectasia?

A

Nevus Flammeus
-known as a “birthmark”

108
Q

Describe Nevus Flammeus

A

Flat lesion of Head and Neck; most regress

109
Q

What is Port Wine Stain?

A

-Form of Nevus Flammeus that grows with the child without regression; often thickens
-Occasionally associated with Sturge-Weber syndrome (mental retardation, vascular changes involving the brain)

110
Q

Describe Spider Telangiectasia

A

-Vascular lesion looks like a spider- central red area with fine, radial projections
-Non-neoplastic

111
Q

Describe Hereditary Hemorrhagic Telangiectasia (HHT)

A

-Autosomal dominant disorder
-Vascular malformations (dilated capillaries/veins) present from birth on skin and mucous membranes
-Can cause serious epistaxis, GI bleeding or hematuria

General Pathology (32 decks)

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