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OS2 - Cardio > Vessel Diseases > Flashcards

Vessel Diseases Flashcards

1
Q

Describe the exogenous and endogenous lipoprotein metabolism pathways.

A

cholesterol from the diet is packaged into chylomicrons in the gut containing ApoB-48, ApoC and ApoE. This gives off FAs to muscle and adipose then goes to the liver. The liver sends out VLDL with ApoB-100 to pick up lipids from the periphery and the lipoprotein becomes IDL, even more pick up becomes LDL and that is uptaken by the liver and peripheral tissues.

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2
Q

Primary chylomicronemia

A

Defective removal of chylomicrons due to ApoC-II and LPL defect. Seen as elevated chylomicrons & VLDL, plus pancreatitis.

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3
Q

Familial hypertriglyceridemia

A

Defective metabolism of VLDL due to LPL defect. Seen as elevated VLDL & triglycerides, plus pancreatitis.

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4
Q

Familial dysbetalipoproteinemia.

A

Defective metabolism of VLDL and chylomicrons due to ApoE defect (E2/E2 alleles, causes decreased binding of E to its liver receptors). Seen as elevated VLDL and chylomicron remnants (IDL); elevated cholesterol and triglycerides 1:1 ratio; plus atherosclerosis.

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5
Q

Familial Combined Hyperlipidemia (FCH)

A

Overproduction of ApoB (means more VLDL). Seen as elevated VLDL, LDL, or both; also premature atherosclerosis.

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6
Q

Familial Hypercholesterolemia (FH)

A

Decreased receptor-mediated removal of LDL from plasma due to defective LDL receptor and ApoB. Seen as increased LDL and premature atherosclerosis.

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7
Q

What is the desirable range for cholesterol levels?

A

Total Cholesterol - 40, Women >50

Triglycerides -

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8
Q

Xanthoma

A

cutaneous manifestations of lipidosis, an accumulation of lipids in foam cells within the skin; associated with hyperlipidemias

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9
Q

Fibromuscular dysplasia

A

Focal irregular artery wall thickening with intimal and medial hyperplasia and fibrosis, leading to luminal stenosis. Typically in renal, carotid, splanchnic, or vertebral arteries; young women.

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10
Q

Hyperplastic arteriolosclerosis

A

*smooth muscle growth
concentric wall thickening due to hyperplasia and hypertrophy of the smooth muscle cells in the t. media (onion layers), also thickened reduplicated basement membrane

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11
Q

Hyaline arteriolosclerosis

A

*protein leak + ECM secretion
wall thickening due to leakage of plasma proteins from lumen into wall, as well as ECM secretion by smooth muscle cells. Caused by HTN.

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12
Q

Fibrinoid change (±necrosis)

A

*protein leak
Wall thickening due to leakage of plasma protein into wall with or without necrosis; often associated with vasculitis so will see surrounding inflammation as well

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13
Q

Medial calcific sclerosis

A

*calcium in elastic lamina

Calcification of internal elastic lamina spreading into tunica media

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14
Q

Atherosclerosis

A

thickening of tunica intima due to lipid accumulation, chronic inflammation, and repair response. This is a chronic inflammatory disease of response to endothelial cell injury.

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15
Q

SHODDY

A

five major modifiable risk factors for atherosclerosis: Smoking, Hypertension, Obesity, Diabetes, DYsplipidemia
+Inflammation/CRP

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16
Q

Pathogenesis of atherosclerosis/plaque formation

A
  1. malfunction of injured endothelial cells (HLD, HGlu, HTN, etc) –> increased permeability, cell adhesion
  2. lipoproteins (LDL and oxidized LDL, cholesterol, and C-esters) accumulation in intima
  3. leukocytes/monocytes come to intima to help, become MPs and [dysfunctional] foam cells (take up too much LDL/lipid)
  4. factors released (from plt, MPs, and endo cells) that recruit smooth muscle cells and T cells
  5. smooth muscle cell proliferation (PDGF, FGF, TGF-alpha) with ECM/collagen deposition
    * then: inflammatory cells may initiate breakdown of ECM and lead to plaque break-off; often undergo calcification
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17
Q

Mechanism by which HLD contributes to atherogenesis

A
  • impairs endo cell function by increasing ROS production when lipids are oxidized
  • free radicals cause membrane and mitochondrial damage, as well as accelerate NO decay (decreased vasodilation effect)
  • ROS/oxidized lipids are scavenged by MPs but there’s no feedback in this system so that’s how foam cells form; smooth muscle cells can also take up lots of lipid
  • the modified lipids can’t be degraded so they sit within cells and cytokines are released –> inflammation/problems
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18
Q

Atherosclerotic plaques have 3 main components:

A
  1. cells - smooth muscle, MP, T cells
  2. ECM - collagen, elastic fibers, PGs
  3. lipid - IC and EC
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19
Q 
What is contained in the:
- fibrous cap
- necrotic core
- periphery
of an atherosclerotic plaque?
A

Cap: smooth muscle cells and relatively dense collagen
Core: lipid, dead cell debris, foam cells, fibrin, thrombus, plasma proteins, EC cholesterol crystals
Periphery: neovascularization (weak, prone to rupture)

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20
Q

Difference between lesion, fatty streak, intermediate lesion, atheroma, fibroatheroma, and complicated lesion.

A

Lesion - histologically normal but with MPs and some foam cells
Fatty streak - IC lipid accumulation
Intermediate lesion - fatty streak with EC lipid pools
Atheroma - IC lipid and core of EC lipid
Fibroatheroma - 1/more lipid cores, fibrotic/calcific layers, increased smooth muscle/collagen
Complicated lesion - surface defect, hematoma/hemorrhage, thrombosis

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21
Q

Vulnerable plaque

A

thin fibrous cap overlying the lipid core of atheroma (as opposed to stable plaque, which has a thick fibrous cap)

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22
Q

Intraplaque hemorrhage

A

blood within the lipid core that got there either by rupture of the neovessels or rupture of the fibrous cap; this may expand the plaque or induce plaque rupture

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23
Q

Plaque rupture

A

break in fibrotic cap that allows communication of core contents with circulation, causing thrombus formation

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24
Q

The most extensively involved vessels in atherosclerosis (in order) are:

A
  1. aorta (lower abdominal)
  2. coronary arteries
  3. popliteal arteries
  4. cerebral arteries
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25
Q

Atherosclerotic stenosis

A

Critical stenosis (enough to cause tissue ischemia) is 70% decrease in cross-sectional area of the lumen. Prior to that the artery will remodel/expand outward to accommodate the plaque build up while not reducing the lumen size. The effects of vascular occlusion depend on the metabolic demand of the affected tissue as well as the arterial supply

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26
Q

Stable angina

A

predictable chest pain with a fixed amount of exertion

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27
Q

Acute plaque changes fall into 3 categories:

A
  1. rupture - release thrombus
  2. erosion - exposing thrombogenic SEC to blood
  3. hemorrhage - expands volume of atheroma
    * adrenergic stimulation associated with circadian waking and emotional stress can contribute to plaque disruption
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28
Q

Potential causes of acute coronary syndromes

A
  • thrombosis formed on disrupted plaque
  • thromboemboli in coronary artery
  • vasoconstriction which decreases lumen and potentiates plaque disruption (can be stimulated by adrenergic agonists, platelet content release, endothelial cell dysfunction, perivascular inflammatory cells’ mediator release)
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29
Q

Dissection

A

tear in the tunica intima that lets luminal blood get in between the intima and media where it tunnels out a second lumen

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30
Q

Ectasia

A

non-discrete, non-localized dilatation (often tortuous) of blood vessel or duct

31
Q

Marfan syndrome

A

defective fibrillin from AD mutation in FBN1 gene, as well as excessive TGF-beta activation, leading to tall thin body and aortic dissections. Treat with beta-blockers (to reduce HR, BP, and aortic wall stress) and new promise in angiotensin-2 receptor blockers

32
Q

Ehlers-Danlos syndrome

A

group of AD hereditary disorders that result in defects in collagen synthesis or structure of fibrillar collagen; COL3A1 gene mutation (for type III collagen) that results in vessels rich in type 3 collagen

33
Q

Cystic medial degeneration

A

loss of smooth muscle cells, collagen, and elastic fibers in tunica media of large arteries leaving cystic areas of myxoid matrix; may or may not see necrosis and may be due to inherited AD disorder or aging.
Will see an interruption in the media that is without muscle cells and collagen/elastin.

34
Q

Pathogenesis of aortic aneurysms

A

interplay between atherosclerosis and genetically determined degeneration of tunica media; increased MMPs with/without decreased tissue MMP inhibitors, spillover inflammation from athero.
Can also be due to genetic defect in fibrillin or collage, infection, or vasculitis.
Most common in abdomen; thrombus usually forms within the aneurysm; symptoms are rare but may be back pain especially if leaking, increased risk of rupture with increased size. Diagnose with imaging (TEE, CT, MRI), treat with stent or open repair.

35
Q

Aortic aneurysm complications

A
  1. Rupture
  2. Mural thrombus formation
  3. Embolism
  4. Obstruction of branches
  5. Aortoenteric fistula
36
Q

Symptoms of aortic aneurysm rupture

A

sudden severe sharp tearing chest pain that moves as the dissection progresses.
Type A = anterior pain
Type B = between scapulas
Arm pain - subclavian; AMS - carotid; collapse - full rupture (into pericardium or–less often–into left pleural cavity)

37
Q

Vasculitis

A

inflammation of blood vessels, mostly autoimmune, mostly treatable, can also be infectious and non-infectious.
Symptoms include fever, myalgia, arthralgia, malaise, palpable purpura, swollen tender artery, HA and scalp tenderness, visual disturbances (can cause blindness), and many more - must think of vasculitis in order to think to look for it

38
Q

Types of arteritis

A

Giant cell = aorta & large/med arteries
Polyarteritis nodosa = large/med & small arteries
ANCA-associated vasculitis = small arteries to veins

39
Q

Pathogenesis of temporal arteritis

A 
"giant cell" arteritis/vasculitis means that destructive inflammation (which is segmental, mural, and granulomatous) creates multinucleated giant cells that attack calcified IEL in big arteries. 
Immune response (innate and adaptive) is initiated by dendritic cells which leads to IL/IFN-gamma secretion for LC attraction and subsequent intimal thickening, cell proliferation, and luminal stenosis.
40
Q

Describe the activation & activity of dendritic cells in the pathogenesis of giant cell arteritis

A

They are activated by antigen stimulation. Antigens come from either pathogens or calcification in the vessel wall. Activation occurs through the ligation of TLRs and a second IC messenger which frees NfkappaB for transcription of pro-inflammatory molecules.
Activated DCs then produce lots of IL-12/IL-18/IL-2/IL-6/IFN-gamma, and they stimulate the release of IFN-gamma from T cells.
They also release CCL19 and CCL21 which bind CCR7 and results in arrest of DCs so they are trapped within the arterial wall.

41
Q

What does each cytokine below do in giant cell arteritis?

IL-2, IL-6, IFN-gamma, IL-12, VEGF/PDGF, MMP-2, MMP-9

A

IL-2: pro-inflammatory cytokine secreted by activated DCs
IL-6: pro-inflammatory cytokine secreted by activated DCs
IFN-gamma: pro-inflammatory cytokine secreted by activated DCs; signature cytokine secreted by Th1 cells; induces MPs to become multinucleated giant cells and granulomas
IL-12: secreted by DCs to activate Th1 cells
MMP-2: MMP that destroys elastin
MMP-9: MMP that destroys elastin

42
Q

Effect of corticosteroids on temporal arteritis

A

effective in relieving symptoms and preventing blindness

43
Q

Takayasu arteritis

A
  • young east Asian females; rare
  • pulseless disease - loss of arm pulses, intermittent arm claudication; renovascular HTN, angina pectoris, other non-specific sx (fatigue, fever, HA, seizures, N/V); stenosis of aorta/major branches, SC or aortic bruit
  • inflammation that is segmental, transmural, necrotizing, and loosely granulomatous with MNGC (plus LCs, intimal & adventitial thickening, medial loss/thinning of elastin, luminal stenosis)
  • treat with corticosteroids and cytotoxic immunosuppressive therapy; prognosis not good
44
Q

Polyarteritis nodosa

A
  • typically white males in 40s
  • neuropathy, renal failure, acute abdomen, cholecystitis, pancreatitis, angina pectoris, livedo reticularis (non-specific), other non-specific symptoms
  • inflammation is segmental, transmural, nodular arteritis with fibrinoid necrosis; neutrophils (ants!) in acute phase with intimal thickening, cell proliferation and degeneration, luminal stenosis, then chronic stage with fibroblasts and scarring +/- aneurysms
  • no diagnostic Abs, treat with corticosteroids, cytotoxic immunosuppressive therapy if severe; prognosis good when treated
45
Q

Kawasaki disease

A
  • mucocutaneous lymph node syndrome, typically in east asian 1yo’s
  • fever ≥5 days, plus four of the following: polymorphous rash, bilateral conjunctival injection, cervical lymphadenopathy, extremity changes (erythema, indurative edema in hands/feet, desquamation of fingertips, Beau’s lines), mucous membrane changes (diffuse injection, tongue erythema/fissuring, strawberry tongue)
  • endothelial necrosis, transmural inflammation with NTs/LCs, also aneurysms/thrombosis
  • treat with aspirin and IVIg, prognosis good
46
Q

Microscopic polyangiitis

A

aka “hypersensitivity vasculitis” or “leukocytoclastic vasculitis”

  • a necrotizing vasculitis that affects capillaries, small arterioles, and venules; clinically evident features include hemoptysis, hematuria, proteinuria, bowel pain/bleeding, muscle pain/weakness, palpable purpura
  • antibody responding to antigens like drugs, microorganisms, heterologous proteins, or tumor proteins either get deposited or induce secondary, pathogenic immune responses (P-ANCAs!) and then recruitment/activation of NTs causes damage to vessel wall
47
Q

Granulomatosis with polyangiitis (Wegener’s disease)

A
  • typically whites in 40s
  • necrotizing granulomatous vasculitis of arteries and veins in URT (palate destruction), LRT (cavitating lung lesions), and kidneys (necrotizing vasculitis of interlobar artery, nodular lesions in medulla, glomerulonephritis)
  • treat with corticosteroids plus either: cytotoxic immunosuppressive therapy or targeted therapy (rituximab)
48
Q

Allergic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)

A

triad: asthma, eosinophilia, vasculitis
- path simplified = Wegener’s + MANY eosinophils
- recognize the eosinophils on H&E with red cytoplasm and bilobed nucleus

49
Q

Buerger disease (Thromboangiitis Obliterans)

A
  • typically young male smokers of MidEast or south Asian ancestry
  • inflammatory thrombosing vaso-occlusive disease of arteries and veins of limbs, present with pain of toes (±fingers) then ischemic ulcers, gangrene, moves distal to proximal
  • path: acute = segmental transmural inflammation without necrosis + thromboses + granulomas + giant cells; chronic = nonspecific organization/recanalization of thrombus + neovascularization + fibrosis
  • treat: stop smoking, amputate gangrene
50
Q

Peripheral artery disease

A
  • chronic atherosclerotic occlusive disease of large and medium arteries, primarily of the legs; common (more so in men) and typically in elderly
  • sx: limb pain (calves) potentiated by exercise; signs include lost pulses, bruit (flow over lesions), pallor/cyanosis, skin/muscle atrophy, ulceration, necrosis
51
Q

Acute arterial occlusion

A
  • uncommon, usually due to thromboemboli, 80% from heart
  • 5 P’s: pallor, paralysis, paresthesia, pulselessness; 70% in legs/10% in brain
  • treat: anticoagulation, IA therapy, thrombectomy, surgery
52
Q

Cardiac Raynaud

A

a coronary artery hyper-reactivity that can cause a syndrome of chest pain same as atherosclerotic CAD, and coronary vasospasm which results in myocardial contraction band necrosis

53
Q

Contraction banding

A

transverse bands of hypercontracted sarcomeres due to calcium influx (causes contraction) after ATP has been depleted (prevents relaxation); this occurs in reperfusion of dead myocardium and cardiac biopsies and is caused by coronary vasopasm

54
Q

Prinzmetal angina

A

Also called a “variant form of angina pectoris”. Chest pain that occurs at rest (this is the variance) and is associated with ST-segment elevation. Thought to be caused by by coronary vasospasm (vascular smooth muscle hyperreactivity). More frequent in smokers, Japanese, and those <50yo.

55
Q

Takotsubo cardiomyopathy

A

extreme stress (particularly emotional) can cause coronary artery vasopasm which can lead to MI or sudden cardiac death – broken heart syndrome

56
Q

Kaposi’s sarcoma

A

vascular neoplasm caused by HHV8 that occurs preferentially in cold-exposed areas (nose, toes, feet, etc.); path: virally encoded G protein induces VEGF production, viral homologue of cycD drives proliferation, and multiple viral proteins inhibit p53.

4 forms:

  1. Classic - of the old MidEast/Medit men
  2. Endemic African - non-HIV and can be indolent or aggressive
  3. Transplant-associated - solid organ recipients who are getting T-cell immunosuppression
  4. AIDS-associated - involves lymph nodes and disseminates widely to viscera
57
Q

Describe the evolution of lesions in Kaposi’s sarcoma.

A

Skin patches of red-purple macules composed of irregular endothelial cell-lined vascular spaces with interspersed LCs, plasma cells, and MPs.
Then the lesions become raised plaques of dermal accumulations of jagged vascular channels lined by plump spindle cells. In between are scattered EV erythrocytes, hemosiderin-laden MPs, other cells.
Lesions eventually become nodular with sheets of spindle cells located in dermis/SC tissue with hemorrhage, hemosiderin, and mononuclear inflammation.

58
Q

DVT

A

conventionally divided into proximal and distal (above/below popliteal vein); studies show that only proximal thrombi are associated with clinically significant PE. Rates of DVT higher in men than women.
Best screening test = compare calf measurements, >2cm positive. Tests include Homan’s sign, D-Dimer test, high sensitivity but low specificity, but there’s 99% NPV.
Prolonged immobilization is most important risk factor, but most commonly DVT patients have cancer, followed by hospitalization, surgery, and then major trauma.

59
Q

Venous stasis dermatitis

A
  • presents with erythematous, scaling, eczematous patches on legs, often medial ankle; can also see hyperpigmentation from extravasation of erythrocytes and hemosiderin accumulation
  • causes ulcers that are tender, exudative, shallow, and have granulation base; never found in forefoot or above knee
  • risk factors include obesity, standing occupation, female sex, hx of DVT
60
Q

Difference between arterial and venous ulcers

A 
arterial = painful, punched out/stellate in shape, may be pale or black/yellow 
venous = usually located on medial ankle or calf, are painful/tender, shallow, exudative, granulation base with irregular border
61
Q

Trosseau syndrome

A

migratory thrombophlebitis - a pro-coagulant state induced by tumor coag factors that thromboses in different vascular beds at different times

62
Q

Sturge-Weber syndrome

A

port wine face.
aka encephalotrigeminal angiomatosis - congenital disorder with facial port wine nevi, ipsilateral venous angiomas in cortical leptomeninges (arachnoid+pia maters), mental retardation, seizures, hemiplegia, radiopacities of skull

63
Q

Superior vena cava syndrome

A

neoplasms (often lung cancer or lymphoma) that compress or invade the SVC and cause obstruction that produces marked dilation of veins in neck, head, arms, and is associated with cyanosis

64
Q

Osler-Weber-Rendu disease

A

aka Hereditary hemorrhagic telangiectasia - AD disorder caused by mutations in genes for TGF-beta signaling pathway in endothelial cells; the telangiectasia lesions can spontaneously rupture causing serious bleeding (nosebleeds, GI bleds, hematuria)

65
Q

Inferior vena cava syndrome

A

neoplasms/thrombi that compress or invade the IVC and cause obstruction that produces marked edema in lower extremities and distention of the superficial collateral veins of the lower abdomen

66
Q

Portal vein hypertension

A

caused by liver cirrhosis, portal vein obstruction, or hepatic vein thrombosis; leads to opening of porto-systemic shunts and increased blood flow into systemic circulation at the GE junction/forms esophageal varices (most important! prone to rupture and fatal GI hemorrhage), at rectum/hemorrhoids, at periumbilical vein/caput medusae

67
Q

contraction band necrosis

A

when cardiac myocytes run out of ATP (such as in ischemia/infarction/necrosis) and then are exposed to influx of calcium (such as in reperfusion), there is an enhanced actin-myosin interaction which results in hypercontraction; this occurs in reperfusion of dead myocardium and also in cardiac biopsies.
On special stain will see highlighted the transverse bands of hypercontracted sarcomeres

68
Q

Caput medusae

A

apparent periumbilicus veins that are a reopening of the umbilical vein due to portal hypertension

69
Q

Homans sign

A

calf pain upon dorsiflexion of foot means positive Homans sign; problem with this is it’s not very sensitive or specific and can actually dislodge the clot

70
Q

Chylothorax

A

A type of pleural effusion; results from lymph formed in the digestive system (called chyle) accumulating in the pleural cavity due to either disruption or obstruction of the thoracic duct.

71
Q

pyogenic granuloma

A

misnomer - capillary angioma, often found in the head mucosa (gums, mouth, nasal region, etc.)

72
Q

bacillary angiomatosis

A

angiomatosis (non-neoplastic growths consisting of many angiomas, or capillary growths) associated with bartonella bacteria

73
Q

angiosarcoma

A

malignant neoplasm of endothelial-type cells; can be associated with lymph vessels or blood vessels (lymphangiosarcoma or hemangiosarcoma)

74
Q

coronary artery vasospasm

A

can be due to hyper-reactivity of blood vessels (sometimes called cardiac Raynaud) and can cause contraction band necrosis and angina pectoris indistinguishable from that of atherosclerotic CAD

OS2 - Cardio (6 decks)

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