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Neoplasm: - Terms
Neoplasm: - Terms
• Terms
Atypia, Differentiation of tumor, Cochexia
Dysplasia, Carcinoma in situ, CIN, R-S cell
Precancerous lesion
Definition:
a persistent elevation of blood pressure to
greater than 140 mmHg systolic, and/or
greater than 90 mmHg diastolic.
Secondary hypertension:
Elevation of blood pressure due to a preceding
defined disease process cause
< 10% of hypertension
The pathogenesis:
1. Genetic susceptibility
familial incidence
2. Sodium homeostasis
high dietary intake of sodium sodium
retention ﹝-﹞Na+-K+ ATPase
intracellular Ca2+↑
3. Cytosol Ca2+ ↑→vascular smooth muscle
constriction ( inhibited by calcium
channel-blocking drugs)
4. Abnormalities of renin, angiotensin and
aldosterone
5. Sympathetic nervous over activation stress
– catecholamines
6. Abnormality in the NO system
NO vasodilation
• (NO donor are effective)
Secondary hypertension :
Many factors →increase cardiac output or peripheral
resistance.
Accentuation of some factors:
renin, aldosterone, renalsodium reabsorption,
catecholamines, sympathetic stimulation
e.g.
• Renal disease: renal artery stenosis (renin)
• Endocrine causes: adrenal tumors( aldosterone )
Clinical features
Benign Hypertension:
A. Early hypertension
no clinical symptom, detecting elevation of BP
(vasoconstriction)
after a long course of sustained hypertension
Vasculature injury
• Functional disturbance
• Vasculature injury
• Organ injury
( 1 ) Functional disturbance
arteriolar wall is
hyalinized, and the
lumen is markedly
narrowed.
Thickening of muscular arteries
Smooth muscle
proliferation of the media
collagen and elastic
fibrous proliferation of
the Intima
②cerebral softening
microinfarct (lacunar infarct)
③cerebral hemorrhage
large fatal
microaneurysm
slit hemorrhages
Blood supply of the brain
Hypertensive hemorrhage of the brain
massive hemorrhage and extended into the lateral ventricle.
• Hypertensive encephalopathy
very high BP→ spasm of small arteries in
the brain – cerebral edema--- sever
headache and transient cerebral dysfunction
• Hypertensive Retinal Disease
• Funduscopic examination
--Increased in the arteriolar light reflex
--Arteriolar-venular crossing defects (arteriovenous
nicking)
--Retinal hemorrhages, exudates and papilledema.
There is arteriolar narrowing and "cotton wool" spots.
Papilledema is shown here. Note that the margins of the optic disk are
indistinct with blurring, because there is swelling with elevation of the
optic nerve head.
Malignant Hypertension
Fibrinoid necrosis
of arterioles
(necrotizing
arteriolitis)
Eosinophilic
granular change in
the wall
fibrinoid necrosis of a small artery
Hyperplastic arteriolosclerosis The wall of arteriole
show onionskin thickening.
consequences
• Hematuria and renal failure due to fibrinoid
necrosis of glomeruli and arteries.
• Cardiac failure
Host antigens
(normal protein present in the heart, joint and other tissues)
Type II hypersensitivity mediated by cross-reacting Ab
Type III hypersensitivity to Streptococal mediated by immune complexs
Pathology
A. Early Phase (exudative, degenerative) 1-4 weeks
multisystem– heart, synovium, joints, skin.
focal fibrinoid necrosis
diffuse cellular infiltration or localized aggregation of cells
Aschoff cells are large, abundant cytoplasm and central round to ovoid
nuclei in which the chromatin is disposed in a central, resembling an owl-
eyed appearance in cross section
C. Fibrosis phase (healed phase) 3-4 month
Aschoff bodies are replaced by fibrous scar
the cytoplasm of the component cell become
spindle shaped and collagenous fibers fuse to
small scars.
Common in cardiac tissue
Fibrosis---The Aschoff body is replaced by a nodule of scar.
Rheumatic Fever
an acute, immune-mediated, multisystem inflammatory
disease
Affects:
Heart: pericarditis, myocarditis and endocarditis --
pancarditis
Joints: polyarthritis
Skin: subcutaneous nodules and skin rashes
Arteries: arteritis
Rheumatic pathologic changes in the organs
--Arthritis
• Affecting large joint (ankle, knees, wrist) , the inflammation
tends to move from joint to joint --- migratory polyarthritis
• subcutaneous nodules :
small subcutaneous palpable nodules.
in the over bony prominence
indicate concurrent cardiac involvement
--Chorea
Random involuntary movement.
involvement of basal ganglia of the brain
has a excellent progress
--Carditis
Most serious manifestation
35% of patients with a first attack of RF
Organization, fibrosis
thickening, shortening,
commissural fusion of
leaflets and tendinous
cord
Chronic rheumatic heart disease
• Characterized by organization of the acute endocardial
inflammation and subsequent deforming fibrosis.
ATH lesion:
• The Fatty streak
• The Fibrous atheromatous plaque
• The complicated lesion
1. Fatty streak
aorta
Histological feature
intimal thicken; many foamy cells
2. The fibrous atheromatous plaque
•Gross:
•Yellow-white elevation
•Cut section--- center of the plaque --- semisolid
yellow material (porridge)
•Most common sites: abdominal aorta
coronary, carotid, vertebrobasilar, mesentric,
renal,
iliofemoral arteris
Gross view
yellow-White
plaque along the
vessel length.
Fibrous cap
LM:
• fibrous cap
a layer of fibrous connective tissue
dense collagen scattered SMCs and macrophages
• Lipid zone
Foam cells (lipid-laden macrophages and SMCs)
extracellular lipid and debris
Needle-shaped cholesterol crystals
• Basal zone
Proliferated SMCs and connective tissue
Fibrous cap
Foamy cell
Raised focal lesion with a soft yellow grumous core of lipid and
covered by a firm, gray fibrous cap.
Atheromatous plaque
A thickend and
hyalined fibrous cap.
Amorphous pink
staining core with
cholesterol clefts.
Granulation tissue can
be seen by the core,
some foamy cells.The
internal elastic lamina
is destroyed and the
media of artery
becomes thinner.
a high magnification of the aortic atheroma
with foam cells and cholesterol clefts.
3.The Complicated plaque
• Thrombosis may cause complete occlusion
caused by – slowing and turbulence of blood
– ulceration of the plaque
• Ulceration
may cause thrombosis
discharge the lipid contents of the plaque
• Dystrophic calcification
in the lipid zone of the plaque, very common
• Vascularization
ingrowth of poorly supported vessels
• Hemorrhage
plaque rupture--- hemorrhage---occlusion of
small blood vessels,
ulceration and thrombosis
• Aneurysm
abdominal aorta
arteries weakened by extensive plaque
formation
Ulceration and thrombosis
ulceration of the luminal surface with rupture of the plaque
aneurysm
This large abdominal atherosclerotic aortic aneurysm has
been opened to reveal abundant layered mural thrombus
within the aneurysm.
calcification
Definition:
An area of myocardial necrosis caused by
local ischemia.
Distribution of infarction:
The left ventrical, interventricular septum,
and conducting system.
A—posterolateral infarct: occlusion of the left circumflex artery.
B—anterior infarct: occlusion of the anterior descending branch of the left
coronary artery.
C—posterior infarct occlusion of the right coronary artery.
Transmural infarct--- ischemic necrosis involves the full
thickness of the ventricular wall.
Subendocardial infarct--- ischemic necrosis limited to the
inner one-third of the ventricular wall.
Left ventricular infarction
ventricular infarction
Microscopic view of a recent myocardial infarction.