Upload
louis-fortunato
View
219
Download
0
Embed Size (px)
Citation preview
7/27/2019 Ch11 Vessels 1
1/119
Diseases of BLOOD VESSELS
7/27/2019 Ch11 Vessels 1
2/119
7/27/2019 Ch11 Vessels 1
3/119
COMPONENTS Intima, Media, Adventitia, M>A or A>M
ENDOTHELIUM
INTERNAL ELASTIC LAMINA ECM: Elastin (~aging) S/D, collagen,
mucopolysaccharides
Smooth Muscle
Connective Tissue
Fat
7/27/2019 Ch11 Vessels 1
4/119
1) Blockage
(preceded by
narrowing)
2) Rupture
Preceded by
weakening)
7/27/2019 Ch11 Vessels 1
5/119
TOPICS Vascular wall
responses
Congenital
Anomalies
Atherosclerosis
Arteriosclerosis Hypertension
Aneurysms
Vasculitides
Raynaud
phenomenon
Veins
Lymphatics
Tumors Interventions
7/27/2019 Ch11 Vessels 1
6/119
DEFINITIONS ARTERIO-sclerosis
ATHERO-sclerosis
Aneurysm
Dissection
Thrombus
Hypertension
Vasculitis/Vasculitides, infectious/NON-infectious (often-autoimmune)
Varicosity
DVT/Thrombo-phlebitis/Phlebo-thrombosis
7/27/2019 Ch11 Vessels 1
7/119
DEFINITIONS Lymphangitis
Lymphedema
Angioma/Hemangioma (generic)
Lymphangioma
Angiosarcoma (generic)
Lymphangiosarcoma
7/27/2019 Ch11 Vessels 1
8/119
NON-Specific Vascular Wall
Response to Injury
Endothelial activation
Smooth Muscle cell roles
Development, Growth,
Remodeling
Intimal thickening
7/27/2019 Ch11 Vessels 1
9/119
ENDOTHELIAL CELLS Recall Jeckyl/Hyde concept: maintain hemostasis/cause
thrombosis
Maintenance of Permeability Barrier
Elaboration of Anticoagulant, Antithrombotic, FibrinolyticRegulators J: Prostacyclin, Thrombomodulin, Heparin, Plasminogen
Elaboration of Prothrombotic Molecules H:vWF, TF,Plasminogen activator inhibitor
Extracellular Matrix Production (collagen, proteoglycans)
Modulation of Blood Flow and Vascular Reactivity
Vasoconstrictors: endothelin, ACE Vasodilators: NO, Prostacyclin
Regulation of Inflammation and Immunity
Regulation of Cell Growth
Oxidation of LDL
7/27/2019 Ch11 Vessels 1
10/119
ENDOTHELIAL CELL
ACTIVATORS Cytokines, GFs
Bacterial Products
Hemodynamic Forces Lipid Products
Viruses
Complement
Hypoxia
Cigarette smoke
7/27/2019 Ch11 Vessels 1
11/119
VASCULAR SMOOTH MUSCLE
Vasoconstriction
Vasodilatation
Make ECM:
Collagen
Elastin
Proteoglycans
Regulated by:
PROMOTORS: PDGF, endothelin, thrombin,
FGF, etc.
INHIBITORS: Heparan SO4, NO, TGF-
7/27/2019 Ch11 Vessels 1
12/119
Vessel Growth
& Remodeling The sum total of all the factors and
processes involved in tissue injury
and the bodys ability to growvessels, develop new pathways,
and re-perfuse areas in response
to tissue and/or blood vesselinjury.
7/27/2019 Ch11 Vessels 1
13/119
7/27/2019 Ch11 Vessels 1
14/119
CONGENITAL ANOMALIES Arteriovenous fistulas
Also called ArterioVenous Malformation
(AVM)
Common factor is abnormal communication
between high pressure arteries and lowpressure veins
Usually congenital (malformation), but can
be acquired by trauma or inflammation
Most often described in the brain as an AVM
Often asymptomatic or with hemorrhage or
pressure effects
7/27/2019 Ch11 Vessels 1
15/119
7/27/2019 Ch11 Vessels 1
16/119
ARTERIO-SCLEROSIS
GENERIC term for ANYTHINGwhich HARDENS arteries
Atherosclerosis (99%)
Mnckeberg medial calcific
sclerosis (1%)
Arteriolosclerosis, involving smallarteries and arterioles, generally
regarded as NOT strictly being part
of atherosclerosis, but more relatedto hypertension and/or diabetes
7/27/2019 Ch11 Vessels 1
17/119
ATHEROSCLEROSIS
(classical) Etiology/Risk Factors
Pathogenesis
Morphology
Clinical Expression
7/27/2019 Ch11 Vessels 1
18/119
ATHEROSCLEROSIS
(ala Robbins) *Natural History
*Epidemiology
*Risk Factors
*Pathogenesis
*Other Factors
*Effects
*Prevention
7/27/2019 Ch11 Vessels 1
19/119
*NATURALHISTORY
7/27/2019 Ch11 Vessels 1
20/119
1) FATTY
STREAK
(non-
palpable,
but a
visible
YELLOW
streak)
2) ATHEROMA
(plaque)
(palpable)
3) THROMBUS
(non-
functional,
symptomatic)
7/27/2019 Ch11 Vessels 1
21/119
7/27/2019 Ch11 Vessels 1
22/119
MORPHOLOGIC CONCEPTS
Macrophages (really monocytes) infiltrate
Intimal Thickening Lipid Accumulation Streak Atheroma Smooth Muscle Hyperplasia and Migration Fibrosis Calcification Aneurysm*
Thrombosis
7/27/2019 Ch11 Vessels 1
23/119
FATTY
STREAKS
7/27/2019 Ch11 Vessels 1
24/119
PLAQUE
7/27/2019 Ch11 Vessels 1
25/119
MILD ADVANCED
7/27/2019 Ch11 Vessels 1
26/119
ADVANCED FEATURES
RUPTURE
ULCERATION
EROSION ATHEROEMBOLI
HEMORRHAGE
THROMBOSIS
ANEURYSM
7/27/2019 Ch11 Vessels 1
27/119
FUN THINGS TO FIND:
Lumen, Fibrous cap (fibrous plaque), Lipid core,External Elastic Membrane thinning/destruction,
Calcification, Neovascularization
7/27/2019 Ch11 Vessels 1
28/119
*EPIDEMIOLOGY
& RISK FACTORS
7/27/2019 Ch11 Vessels 1
29/119
Epid./RiskFactors
Related to development of nation
US highest
50-70% DECREASE 19632000. Why?awareness, dietary restrictions
AGE
SEX, M>F until menopause, estrogen
protection
GENETICS (multigenic)
7/27/2019 Ch11 Vessels 1
30/119
MAJORfactors
Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Milletus
7/27/2019 Ch11 Vessels 1
31/119
Risk Factors for Atherosclerosis
Major MinorNON-modif iable Modif iable
Increasing age Obesity
Male gender Physical inactivity
Family history Stress ("type A" personality)
Genetic abnormalities Postmenopausal estrogen deficiency
High carbohydrate intake
Modif iable
Hyperlipidemia Alcohol
Hypertension Lipoprotein Lp(a)
Cigarette smoking Hardened (trans)unsaturated fat intake
Diabetes Chlamydia pneumoniae
7/27/2019 Ch11 Vessels 1
32/119
MAJORfactors
Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Milletus
7/27/2019 Ch11 Vessels 1
33/119
HYPERLIPIDEMIA Chiefly CHOLESTEROL,
LDL>>>>HDL
HDL mobilizes cholesterol FROMatheromas to liver
LOW CHOLESTEROL diet is GOOD
UNSATURATED fatty acids GOOD
Omega-3 fatty acids GOOD
Exercise GOOD
7/27/2019 Ch11 Vessels 1
34/119
Foamy MACROPHAGES
7/27/2019 Ch11 Vessels 1
35/119
CHOLESTEROL* CLEFTS
*Really cholesterol esters
7/27/2019 Ch11 Vessels 1
36/119
7/27/2019 Ch11 Vessels 1
37/119
HYPERTENSION HYPERTENSION causes
ATHEROSCLEROSIS. Why?
ATHEROSCLEROSIS causesHYPERTENSION. Why?
7/27/2019 Ch11 Vessels 1
38/119
CIGARETTES What more needs to be said?
7/27/2019 Ch11 Vessels 1
39/119
DIABETES If there was one disease
which I could challenge youto, as a dare, to PROVE tome that was NOT EXACTLY
THE SAME asatherosclerosis, it would beDIABETES! Any takers?
7/27/2019 Ch11 Vessels 1
40/119
NON major factors
Homocysteinuria/homocysteinemia, relatedto low B6 and folate intake
Coagulation defects
Lipoprotein Lp(a), independent ofcholesterol. Lp(a) is an altered form of LDL
Inadequate exercise, Type A personality,
obesity (independent of diabetes) Protective effect of moderate alcohol?
Medical LIE, sponsored by the booze
industry and alcoholic physicians!
7/27/2019 Ch11 Vessels 1
41/119
PATHOGENESIS
atherosclerosis is a chronic
in f lammatory response of
the arterial wal l ini t iated byinjury to the endothelium
7/27/2019 Ch11 Vessels 1
42/119
PATHOGENESIS SAGA
Chronic endothelial injury LDL, Cholesterol in arterial WALL OXIDATION of lipoproteins Monocytes migrate endothelium* Platelet adhesion and activation Migration of SMOOTH MUSCLE from media to
intima to activate macrophages (foam cells) Proliferation of SMOOTH MUSCLE and ECM Accumulation of lipids in cells and ECM
7/27/2019 Ch11 Vessels 1
43/119
M i FOUR STARS f
7/27/2019 Ch11 Vessels 1
44/119
Main FOUR STARS of
PATHOGENESIS SAGA
1) Endothelial Injury 2) Inflammation
3) Lipids
4) Smooth Muscle Cells, SMCs
7/27/2019 Ch11 Vessels 1
45/119
7/27/2019 Ch11 Vessels 1
46/119
Other Pathogenesis
Considerations Oligoclonality of cells in
plaque
Chlamydia, CMV as
endothelial injurers
7/27/2019 Ch11 Vessels 1
47/119
PREVENTION PRINCIPLES
Know what is preventable
Know what is MAJOR (vs. minor)
Know PRIMARY vs. SECONDARY
principles Understand atherosclerosis begins in
CHILDHOOD
Risk factors in CHILDREN predict theADULT profile
Understand SEX, ETHNIC differences
C th l i
7/27/2019 Ch11 Vessels 1
48/119
Can atherosclerosis
be REVERSED?
?
NON ATHEROSCLEROSIS
7/27/2019 Ch11 Vessels 1
49/119
NON ATHEROSCLEROSIS
VASCULAR DISEASES
HYPERTENSION
ANEURYSMSVASCULITIDES
VEIN DISORDERS NEOPLASMS
7/27/2019 Ch11 Vessels 1
50/119
HYPERTENSION
ESSENTIAL 95%
SECONDARY 5%
SECONDARY
7/27/2019 Ch11 Vessels 1
51/119
SECONDARY Renal Acute glomerulonephritis
Chronic renal disease
Polycystic disease
Renal artery stenosis
Renal artery fibromuscular dysplasia
Renal vasculitis
Renin-producing tumors
Endocrine Adrenocortical hyperfunction
(Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oralcontraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidaseinhibitors)
Pheochromocytoma, acromegaly, HYPO-thyroidism (myxedema), HYPER-thyroidism
pregnancy-induced
Cardiovascular: Coarctation of aorta, polyarteritis nodosa (or other vasculitis) Increased intravascular volume
MISC: Increased cardiac output, Rigidity of the aorta, neurologic, Psychogenic,Increased intracranial pressure, sleep apnea, acute stress, including, surgery
7/27/2019 Ch11 Vessels 1
52/119
DEFINITION 140/90
SUSTAINED diastolic >90
SUSTAINED systolic >140
7/27/2019 Ch11 Vessels 1
53/119
BP = CO x PR
ALL Hypertension
7/27/2019 Ch11 Vessels 1
54/119
E.F.
R i A i t i Ald t
7/27/2019 Ch11 Vessels 1
55/119
ReninAngiotensinAldosteroneAXIS (RAAS)
If the perfusion of thejuxtaglomerularapparatus in the kidneys decreases, then the
juxtaglomerular cells release the enzymerenin.
Renin cleaves an inactive peptide calledangiotensinogen, converting it intoangiotensin I.
Angiotensin I is then converted to angiotensinII by angiotensin-converting enzyme (ACE),which is found mainly in lungcapillaries.
Angiotensin II is the major bioactive product ofthe renin-angiotensin system. Angiotensin IIacts as an endocrine, autocrine/ paracrine, and
intracrine hormone.
http://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Reninhttp://en.wikipedia.org/wiki/Peptidehttp://en.wikipedia.org/wiki/Angiotensinogenhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Capillarieshttp://en.wikipedia.org/wiki/Endocrine_systemhttp://en.wikipedia.org/wiki/Autocrine_signallinghttp://en.wikipedia.org/wiki/Paracrine_signallinghttp://en.wikipedia.org/wiki/Intracrinehttp://en.wikipedia.org/wiki/Intracrinehttp://en.wikipedia.org/wiki/Paracrine_signallinghttp://en.wikipedia.org/wiki/Autocrine_signallinghttp://en.wikipedia.org/wiki/Endocrine_systemhttp://en.wikipedia.org/wiki/Capillarieshttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinogenhttp://en.wikipedia.org/wiki/Peptidehttp://en.wikipedia.org/wiki/Reninhttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatus7/27/2019 Ch11 Vessels 1
56/119
7/27/2019 Ch11 Vessels 1
57/119
GENETIC
ACQUIRED
HISTOPATHOLOGY of
7/27/2019 Ch11 Vessels 1
58/119
HISTOPATHOLOGY of
ESSENTIAL HYPERTENSION
HYALINE = BENIGN HTN. HYPERPLASTIC = MALIGNANT HTN. SYS>200
1) ONION SKIN 2) FIBRINOID NECR.
GENETIC
7/27/2019 Ch11 Vessels 1
59/119
GENETICvs.
ENVIRONMENTAL GENETIC UN-CONTROLLABLE ENVIRONMENTAL CONTROLLABLE
STRESS
OBESITY
SMOKING
PHYSICAL ACTIVITY
NaCl INTAKE
ANEURYSMS
7/27/2019 Ch11 Vessels 1
60/119
ANEURYSMS TRUE vs. FALSE
ATHEROSCLEROTIC NON-ATHEROSCLEROTIC
CONGENITAL
LUETIC (SYPHILITIC)
TRAUMATIC
MYCOTIC (MIS-leading term)
2 to VASCULITIS
SACCULAR (i.e., Berry) vs. FUSIFORM
DISSECTION vs. NON-DISSECTION
7/27/2019 Ch11 Vessels 1
61/119
ANEURYSMS
7/27/2019 Ch11 Vessels 1
62/119
ANEURYSMS 2 CAUSES:
1) ATHEROSCLEROSIS 2) CYSTIC MEDIAL DEGENERATION (NECROSIS), can be familial
NORMAL elastic fibers DISRUPTED, FRAGMENTED elastic fibers
7/27/2019 Ch11 Vessels 1
63/119
Most abdominal aortic aneurysms (AAA) occur between
the renal arteries and the bifurcation of the aorta
7/27/2019 Ch11 Vessels 1
64/119
(sequelae)RUPTURE
OBSTRUCTION
EMBOLISM
COMPRESSION
URETER SPINE
MASS EFFECT
THORACIC
7/27/2019 Ch11 Vessels 1
65/119
THORACICANEURYSMS
Encroachment
Respiratory difficulties
Hoarseness?Dysphagia
Cough
PainAortic valve dilatation
Rupture
7/27/2019 Ch11 Vessels 1
66/119
DISSECTION
ANEURYSMS
7/27/2019 Ch11 Vessels 1
67/119
ANEURYSMS
(luetic)Chiefly thoracic
Follows an AORTITIS
PLASMA CELLS predominate
VASCULITIDES
7/27/2019 Ch11 Vessels 1
68/119
VASCULITIDES
TEMPORAL GIANT CELL ARTERITIS TAKAYASU ARTERITIS
POLY (PERI) ARTERITIS NODOSA
KAWASAKI DISEASE
WEGENERs GRANULOMATOSIS
THROMBOANGI(i)TIS OBLITERANS(BUERGER[s] DISEASE)
OTHER
INFECTIOUS
VASCULITIDES
7/27/2019 Ch11 Vessels 1
69/119
VASCULITIDES
Chiefly arterial Infectious (5%) vs. Non-infectious (95%)
NON-infectious are generally AUTO-
IMMUNE. Why? Persistent findings:
Immune complexes
ANTI-NEUTROPHIL ABs (Wegeners, Temporal)
ANTI-ENDOTHELIAL CELL ABs (Kawasaki)
Often DRUG related (Hypersensitivity, e.g.),especially small blood vessels.
TEMPORAL ARTERITIS
7/27/2019 Ch11 Vessels 1
70/119
TEMPORAL ARTERITIS
aka, Giant Cell Arteritis, GCA ADULTS Mainly arteries of the head and
temporal arteries are the most visibly,palpably, and surgically accessible
BLINDNESS most feared sequelae
GRANULOMATOUS WALLinflammation diagnostic
OFTEN associated with marked ESRelevation to be then known asPOLYMYALGIA RHEUMATICA
Anti-NEUTROPHIL ABs often POSITIVE
7/27/2019 Ch11 Vessels 1
71/119
TEMPORAL ARTERITIS
7/27/2019 Ch11 Vessels 1
72/119
TEMPORAL ARTERITIShttp://www.path.
uiowa.edu/cgi-bin-
pub/vs/fpx_gen.
cgi?slide=623&vi
ewer=java&view
=0&lay=iowa
S S
7/27/2019 Ch11 Vessels 1
73/119
TAKAYASU ARTERITIS
Involves aortic arch and other heavilly
elastic arteries, i.e., chief thoracicaorta branches, most commonly young
Asian women
FEMALES
7/27/2019 Ch11 Vessels 1
74/119
POLY-(Peri-) ARTERITIS
7/27/2019 Ch11 Vessels 1
75/119
NODOSA (PAN)
ANY MEDIUM or SMALL artery OFTEN visceral arteries
Infarcts, aneurysms, ischemia
CLASSICAL AUTOIMMUNE disease SEGMENTAL, TRANSMURAL,
NECROTIZING (fibrinoid) inflammation
Sometimes anti-neutrophil antibodies,especially in the smaller vessel diseases
One of the CLASSICAL systemic auto-
immune diseases, like SLE, RA, or SS
http://www
7/27/2019 Ch11 Vessels 1
76/119
.path.uiow
a.edu/cgi-
bin-
pub/vs/fpx
_gen.cgi?s
lide=584&
viewer=jav
a&view=0
&lay=iowa
KAWASAKI DISEASE
7/27/2019 Ch11 Vessels 1
77/119
KAWASAKI DISEASE
CHILDREN
7/27/2019 Ch11 Vessels 1
78/119
HYPERSENSITIVITY VASCULITIS
LEUKOCYTOCLASTIC VASCULITIS
SMALL VESSELS OF ALL TYPES,e.g., capillaries and veins too
FRAGMENTED NEUTROPHILS aka, LEUKOCYTOCLASIA
aka, NUCLEAR DUST
Most are ALLERGIC reactions toallergens like penicillin or strep
DERMATOLOGISTs DISEASE
http://ww
7/27/2019 Ch11 Vessels 1
79/119
http://ww
w.path.ui
owa.edu/
cgi-bin-
pub/vs/fpx_gen.cg
i?slide=6
34&view
er=java&
view=0&l
ay=iowa
WEGENER GRANULOMATOSIS
7/27/2019 Ch11 Vessels 1
80/119
WEGENER GRANULOMATOSIS
M>F, often in 40s
ACUTE NECROTIZING GRANULOMAS OF
UPPER an LOWER respiratory tract
NECROTIZING GRANULOMATOUSVASCULITIS of SMALL vessels of ALL types
Often renal involvement, crescentic
glomerulonephritis
ANTI-NEUTROPHIL-CYTOPLASMIC-ABs
usually present
necrosis
granulomas
7/27/2019 Ch11 Vessels 1
81/119
necrosisgranulomas
necrosis
granulomas
necrosis
granulomas
necrosisgranulomas
necrosisgranulomas
necrosis
granulomas
necrosis
granulomas
necrosisgranulomas
granulomas
necrosis
granulomas
necrosis
granulomasnecrosis
granulomas
THROMBOANGIITIS OBLITERANS
7/27/2019 Ch11 Vessels 1
82/119
THROMBOANGIITIS OBLITERANS
BUERGER(s) Disease
100% caused by cigarette smoking
MEN>>>F, 30s, 40s
Often arteries are 100% obliterated,
hence the name obliterans
EXTREMITIES most often involved
7/27/2019 Ch11 Vessels 1
83/119
http://www.path.uio
wa.edu/cgi-bin-
pub/vs/fpx_gen.cgi
?slide=704&viewer=java&view=0&lay
=iowa
OTHER VASCULITIDES
7/27/2019 Ch11 Vessels 1
84/119
OTHER VASCULITIDES
SLE
RHEUMATOID ARTHRITIS
INFECTIOUS ARTERITIDES
7/27/2019 Ch11 Vessels 1
85/119
INFECTIOUS ARTERITIDES
ASPERGILLIS
MUCORMYCOSIS
MYCOTIC ANEURYSMS aregenerally MISNOMERS
NON ATHEROSCLEROSIS
7/27/2019 Ch11 Vessels 1
86/119
VASCULAR DISEASES HYPERTENSION
ANEURYSMS
VASCULITIDES
VEIN DISORDERS
NEOPLASMS
FINAL TOPICS
7/27/2019 Ch11 Vessels 1
87/119
FINAL TOPICS Raynaud Phenomenon
Veins and Lymphatics Varicosities
Thrombophlebitis/Phlebothrombosis
SVC/IVC syndromes Lymphangitis
Lymphedema
Tumors: Benign, Intermediate(Borderline), Malignant
Vascular Interventions: Angioplasty,Stents, Grafts
R d Ph
7/27/2019 Ch11 Vessels 1
88/119
Raynaud Phenomenon PRIMARY: (formerly Raynaud DISEASE)
Digital PALLORCYANOSISHYPEREMIA (WHITE) (BLUE) (RED) Vasoconstriction usually triggered by COLD, emotion
Can be tip of nose, not only digits Self Limited, Gangrene UN-common
Arteries often do NOT show diagnostic pathology
SECONDARY: (formerly Raynaud Phenomen.)
Atherosclerosos
SLE
Buerger Disease
7/27/2019 Ch11 Vessels 1
89/119
WHITE
BLUE
RED
Varicose Veins
7/27/2019 Ch11 Vessels 1
90/119
Varicose Veins 20% of population, F>M
Related to increased venous pressure, age, valvedysfunction
Superficial veins of lower extremities most
common PATH: 1) DILATED, 2) TORTUOUS, 3) ELONGATED,
4) SCARRED (phlebosclerosis), 5) CALCIFICATIONS,
6) NON-UNIFORM SMOOTH MUSCLE
Conceptually like varices or hemorrhoids
Phlebosclerosis is what your pathologist will
call it
7/27/2019 Ch11 Vessels 1
91/119
THROMBOPHLEBITIS
7/27/2019 Ch11 Vessels 1
92/119
THROMBOPHLEBITIS
90% DEEP veins of the legs IDENTICAL to PHLEBOTHROMBOSIS
Factors: CHF, Neoplasia (esp. GI, panc.
Lung adenocarcinomasmigratorythrombophlebitis), pregnancy, obesity,post-op, immobilization, or any of theparts of Virchows triangle
Sequelae: PE most feared
Symptoms: edema, cyanosis, heat, pain,tenderness, but usually..NONE!!!
SVC SYNDROME
7/27/2019 Ch11 Vessels 1
93/119
SVC SYNDROME
Usually from bronchogenic CAor mediastinal lymphoma
DUSKY CYANOSIS of:Head
Neck
Arms
IVC SYNDROME
7/27/2019 Ch11 Vessels 1
94/119
IVC SYNDROME
Secondary to: NEOPLASMS (external compression)
ASCENDING THROMBOSIS from
FEMORALS, ILIACS
AAA, Gravid uterus
Bilateral leg edema
Massive proteinuria if renal veinsinvolved (like nephrotic syndrome)
LYMPHANGITIS
7/27/2019 Ch11 Vessels 1
95/119
LYMPHANGITIS From regional infections Group-A beta-hemolytic strep most
common
Lymphatics dilated, filled with WBCs Cellulitis usually present too
Lymphadenitis also usually follows
If lymph nodes cannot filter (process)antigens enoughsepticemia
7/27/2019 Ch11 Vessels 1
96/119
LYMPHEDEMA
7/27/2019 Ch11 Vessels 1
97/119
LYMPHEDEMA
Lymphatic channels blocked orscarred or absent:
Post surgical
Post radiationFilaria
Congenital
Tumoral (peau dorange- breast)
7/27/2019 Ch11 Vessels 1
98/119
CHYLE
7/27/2019 Ch11 Vessels 1
99/119
CHYLE CHYLOUS ASCITES
CHYLOTHORAX
CHYLOPERICARDIUM
Vascular TUMORS
7/27/2019 Ch11 Vessels 1
100/119
Vascular TUMORS
BENIGN (NEVER metastasize, in factsome are not even TRUE neoplasms,
but hamartomas)
INTERMEDIATE (rarely metastasize)
MALIGNANT (FREQUENT and EARLYmetastases, like any other sarcomalung)
7/27/2019 Ch11 Vessels 1
101/119
BENIGN---------------------------------------MALIGNANTRare mitosis--------------------------Common mitosisMild, rare atypia------------Frequent, severe atypiaNO mets----------------------------Early, frequent mets
via BLOODSTREAM
HEMANGIOMA
7/27/2019 Ch11 Vessels 1
102/119
HEMANGIOMA Often a generic term for ANY benign blood
vessel tumor
CAPILLARY (small vascular spaces)
Also called juvenile, often called birth marks Usually regress with age
CAVERNOUS (LARGE vascularspaces) Also called adult
Usually do NOT regress
7/27/2019 Ch11 Vessels 1
103/119
PYOGENIC GRANULOMA
7/27/2019 Ch11 Vessels 1
104/119
PYOGENIC GRANULOMA
ORAL CAVITY MOST COMMON
Histology like capillary
hemangioma
Regress
Indistinguishable from normal
granulation tissue
7/27/2019 Ch11 Vessels 1
105/119
LYMPHANGIOMA
7/27/2019 Ch11 Vessels 1
106/119
LYMPHANGIOMA Small 1-2 mm
90% Head and neck region in kids
7/27/2019 Ch11 Vessels 1
107/119
GLOMUS TUMOR
7/27/2019 Ch11 Vessels 1
108/119
GLOMANGIOMA
1 cm
Most commonly under nail
Painful
7/27/2019 Ch11 Vessels 1
109/119
7/27/2019 Ch11 Vessels 1
110/119
MISC. BENIGN TUMORS
7/27/2019 Ch11 Vessels 1
111/119
-ectasias, telangiectasias
Nevus Flammeus, aka, port wine stain----
Spiders (spider telangiectasias), ass. W.
pregnancy, cirrhosis------------------------- Osler-Weber-Rendu Disease (Hereditary
Hemorrhagic Telangiectasia)------------- Bacillary Angiomatosis, in HIV patients,
caused by bacilli of Bartinella species
INTERMEDIATE (BORDERLINE)VASCULAR NEOPLASMS
7/27/2019 Ch11 Vessels 1
112/119
VASCULAR NEOPLASMS
Kaposi Sarcoma, KS 1) Classic European, described 1872, NON-HIV
2) African, pre-HIV, now HIV- and HIV+
3) Transplant associated, HIV-
4) AIDS KS, caused by HHV-8, aka KSHV
PATCH PLAQUENODULE HEMANGIOENDOTHELIOMA*
(HETEROGENEOUS GROUP OFNEOPLASMS)
7/27/2019 Ch11 Vessels 1
113/119
7/27/2019 Ch11 Vessels 1
114/119
Diagnosis of vascular neoplasms may require
the use of endothelial cell markers such as
Factor VIII or CD-31, especially if clear cutvascular spaces are difficult to see, especially if
the tumor is UNDIFFERENTIATED enough to the
degree that endothelial lined spaces are NOT
clearly seen.
MALIGNANT VASCULAR
7/27/2019 Ch11 Vessels 1
115/119
TUMORS
ANGIOSARCOMA May not look vascular at all
Severe atypia
Frequent and often bizarre mitoses
Behave as any sarcoma might, i.e., early
pulmonary metastases
HEMANGIOPERICYTOMA* HETEROGENOUS group of disorders Most commonly arising in pelvic retroperitoneum
VASCULAR INTERVENTIONS
7/27/2019 Ch11 Vessels 1
116/119
VASCULAR INTERVENTIONS
ANGIOPLASTY
STENTS
GRAFTS
Autologous (saphenous v., internal
mammary a.)
Synthetic (Teflon)
ANGIOPLASTIES
7/27/2019 Ch11 Vessels 1
117/119
ANGIOPLASTIES Plaque fracture (crackling sound)
Dissection
Arterial dilatation initially Restenosis ~ 6 months
STENTS
7/27/2019 Ch11 Vessels 1
118/119
STENTS
Metallic mesh Permanently placed
Stays patent longer
than angioplasty OFTEN DRUG COATED
Goals:
Prevent thrombosis Prevent spasm
Delay RE-stenosis
GRAFTS
7/27/2019 Ch11 Vessels 1
119/119
GRAFTS 400,000 CABG grafts per year in USA Saphenous v. vs. Internal mammary a. (internal
thoracic a.)
50% patent after 10 years, for saphenous v. 90% patent after 10 years, for mammary a.
Endothelial and smooth muscle migration andproliferation are key factors for success