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HEMODYNAMICS
Ella C. Lim, M.D., DPSP
EDEMA
Hydrothorax, hydroperitoneum
(ascites), hydropericardium, anasarca
EDEMA
Causes:
LYMPHATIC OBSTRUCTION that
impairs interstitial fluid clearance
(e.g., scarring, tumors- pMRM,
infection - filariasis)
PRIMARYRENAL SODIUM
RETENTION (renal failure)
INCREASED VASCULAR
Lymphatic obstruction from
filariasis
Pitting edema of the leg
Edema
HYPEREMIA & CONGESTION
Lung, acute pulmonary
congestion & edema – medium
power
Identify:
Congested alveolar septa
Intra-alveolar transudate
Edema in inflammation is an
exudate.
Lung, chronic passive venous
congestion – gross
Lung, chronic passive venous
congestion – gross
Identify:
Hilus
Pleura
Cut surface
Hemosiderin
Lung, chronic passive venous
congestion – high power
Identify:
Alveolar
septa
Macrophages with hemosiderin
Dyspnea
Orthopnea
Paroxysmal nocturnal
dyspnea
Cough
Liver, chronic passive venous
congestion – gross, cut surface
Liver, chronic passive venous
congestion – gross, cut surface
This condition is caused by resistance or
obstruction to the outflow of venous
blood from the liver, as may occur in
chronic right heart failure (congestive
heart failure).
The area surrounding the central veins
(centrizonal) becomes intensely
congested, and the hepatocytes in the
central zone may even become necrotic
due to hypoxia.
Liver, chronic passive venous
congestion – gross, cut surface
The alternating pale areas represent
the periportal hepatocytes, which have
sustained a lesser degree of hypoxia.
This gross appearance is also called
NUTMEG LIVER.
Remember that in the hepatic lobules,
blood flows from the periportal to the
central zones, and hence the
centrilobular areas are more
vulnerable to hypoxia than are the
NUTMEG
NUTMEG
Liver, chronic passive venous
congestion – medium power
Liver, chronic passive venous
congestion – medium power
Identify:
Portal triads
Congestion
PETECHIAE & PURPURA
ECCHYMOSES
HEMOSTASIS
Endothelial Injury
Vasoconstriction – Endothelin
Primary Hemostasis – Platelet
adhesion (vWF) – shape change –
granule release (ADP, TXA2) -
recruitment – aggregation (1º
hemostatic plug)
Secondary Hemostasis – TF &
phospholipids (coagulation cascade) –
thrombin activation – fibrin
polymerization – 2º hemostatic plug
COAGULATION CASCADE
Coagulation Cascade
Intrinsic Pathway – Factor XII (Hageman
factor)
Extrinsic Pathway – Tissue Factor
Common Pathway – Factor IX –
Thrombin – Fibrin
Fibrinolytic Cascade
Plasminogen - Plasmin
COAGULATION CASCADE
(2)Antithrombin is activated by
binding to heparin-like molecules on
the endothelium; activated
COAGULATION CASCADE
Heart, coronary artery thrombosis
–
low power
Heart, coronary artery
thrombosis –
low power
Identify:
Intima
Thrombus
Recanaliza
tion
Media
Adventitia
Heart, coronary artery
thrombosis
This cross section of the coronary
artery in the previous image shows
marked concentric thickening of the
intima, due to intimal damage and
subsequent deposition of fibrous
tissue.
On one side, a fresh thrombus is
attached to the damaged
endothelium. In some parts of the
thrombus, there is formation of new
capillary channels. This process, called
THROMBOSIS
Thrombus development depends on the
relative contribution of the components of
Virchow’s triad:
ENDOTHELIAL INJURY (toxins,
Lines of Zahn
Postmortem clot
THROMBOSIS
Venous thrombi – gross, cross
section
Propagation
Embolization
Dissolution
Organization with
recanalization
EMBOLISM
EMBOLISM
Fat embolism – from traumatic
fracture of the long bones and pelvis
CNS damage – ischemia, hemorrhage
Respiratory failure – hypoxemia
Heart, myocardial infarct:
acute vs. healed – gross, cross
section
Identify:
Acute infarct: coagulative necrosis
Brain, cerebral infarct: acute
vs. chronic – gross, coronal
section
Identify: Acute hemorrhagic infarct
Lung, pulmonary infarct – gross,
cut surface
Identify:
Infarct
Pleura
Lung, infarct - medium power
Lung, infarct – high power
Note that the outlines of the
pulmonary alveoli can be seen, but
the structural details have been
obscured in this area of coagulative
necrosis.
There are no intact nuclei. The
pulmonary airspaces seem filled with
debris, derived in this case from
remnants of red blood cells (ie, there
was hemorrhage in this area of
necrosis). This appearance is typical
of pulmonary infarcts.
SHOCK
Other complications:
Multi-organ dysfunction – most
common COD
Kidney, renal tubular necrosis due
to shock – gross, outer & cut
surfaces
Identify:
Cortex
Medulla
Calyces
Kidney, acute tubular necrosis
due to shock – high power
Identify:
Glomeruli
Brain, cortical laminar necrosis
–
gross, coronal section
Identify:
Normal cortex