Hemodynamic disorders. Arterial and venous hyperemia. Hemorrhages. Classification.
Questionary Systemic hemodynamic disorders –
generalized venous hyperemia. Arterial hyperemia and local venous
hyperemia. Hemorrhages. Normal hemostasis. Thrombosis – pathogenesis.
Morphology of thrombus. Evolution. Special features of thrombus
according to the localization. Fate of thrombus.
Normal fluid homeostasis/ Hemodynamic disorders
Normal fluid homeostasis requires
vessel wall integrity maintenance of
intravascular pressure and osmolarity within physiologic ranges
Normal hemostasis Microcirculation
Arterioles, capillaries, venules
Hemodynamic disorders
Hemodynamic disorders
Hyperemia Local inceased blood volume,
congestion Hemorrhages
Blood loss, shock Thrombosis
inappropriate clotting Embolism
migration of clots Ischemia/Infarctus
Obstruction of tissue blood supplies Oedemas
water extravasation into interstitial spaces
The most important causes of morbidity and mortality in Western society
myocardial infarction, pulmonary embolism, and cerebrovascular accident (stroke).
Hyperemia A local increased volume of
blood in a particular tissue Dilatation of small vessels
Two types Arterial (active) hyperemia-
hyperemia from augmented blood flow
due to arteriolar dilation Venous hyperemia-congestion,
cyanosis a passive process resulting
from impaired venous return out of a tissue
closely related to the development of edema
so that congestion and edema commonly occur together
Arterial hyperemia Active process
Due to arteriolar dilatation Sympathic stimulation The affected tissue is redder
than normal because of engorgement with oxygenated blood
Examples at sites of inflammation in skeletal muscle during
exercise Angioneurothic – face redness
Venous hyperemia/congestion
A passive process resulting from impaired venous return out of a tissue.
Two types Systemic, generalized - in cardiac
failure Acute/chronic
Local – in an isolated venous obstruction
The tissue has a blue-red color (cyanosis)
especially in worsening congestion, which leads to accumulation of deoxygenated hemoglobin in the affected tissues
Systemic venous hyperemia
Congestion- a common clinical term
often used interchangeably with the term edema or hyperemia
Heart failure Left-sided heart failure-LUNG
acute chronic
Right-sided heart failure- LIVER acute Chronic
Both sides
Left-sided heart failure=LUNG
The morphologic and clinical effects of left-sided CHF primarily result from the retension of blood within the pulmonary circulation
contractility of left ventricle, unable to eject the blood delivered to it during sistola
The most common causes of left-sided cardiac failure are
(1) CHD, (2) systemic hypertension, (3) mitral or aortic valve disease, and (4) primary diseases of the myocardium
Acute LHF =oedema pulmonum Myocardial infarction
Chronic LHF = induratio fusca pulmonum
Left-sided heart failure=LUNG
Morphology
Macroscopy/Microscopy The extracardiac effects of left-sided
heart failure are manifested most prominently in the lungs.
Acute pulmonary congestion and edema
The lungs are heavy and wet histologically there are perivascular and
interstitial transudate, alveolar septal edema, and intra-alveolar edema
Chronic pulmonary congestion the septa become thickened and fibrotic,
and the alveolar spaces may contain numerous hemosiderin-laden macrophages ("heart failure cells").
Perl’s staining for Fe+ – blue granules
ACUTE PULMONARY EDEMA
Chronic pulmonary congestion = Induratio fusca pulmonum
Heart failure cells -hemosiderin laden macrophages
Right-sided heart failure- LIVER
The major morphologic and clinical effects of pure right-sided heart failure result from the retention of blood within of the systemic and portal venous systems
with hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites.
The most common causes of right-sided cardiac failure are: consequence of left-sided heart failure
any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart
Less common - in chronic pulmonary hypertension (cor pulmonale)
intrinsic disease of lung parenchyma and/or pulmonary vasculature (pulmonic or tricuspid valve disease)
Acute RHF = cyanosis hepatis Embolia a.pulmonalis
Chronic RHF = hepar moshatum
Right-sided heart failure- LIVER
Morphology Macroscopy/Microscopy
Liver and Portal System The liver is usually increased in size
and weight (congestive hepatomegaly)
a cut section displays prominent passive congestion, a pattern referred to as nutmeg liver
congested red centers of the liver lobules are surrounded by paler, sometimes fatty, peripheral regions.
Acute congestion –cyanosis hepatis vv. centrales –dilated (severe
central hypoxia may produce centrilobular necrosis) and sinusoidal congestion.
Chronic congestion- hepar moshatum
With long-standing severe right-sided heart failure, the central areas can become fibrotic, creating so-called cardiac cirrhosis
Liver –acute/chronic congestion
ACUTE/CHRONIC PASSIVE HYPEREMIA LIVER
Cyanosis hepatis/Hepar Moschatum
• Necrosis in the cental part of the hepatic lobule, statosis – in the middle part and no change in periportal part• can progress to cirrohisis – cardiac cirrhosis
dilated vv. centrales and sinusoidal congestion
Right-sided heart failureMorphology
Right-sided heart failure also leads to elevated pressure in the portal vein other organs and transudate
congestive splenomegaly enlarged spleen, can achieve weights of 300 to
500 gm (normal <150 gm). Microscopically, there can be marked sinusoidal
dilation. Congestive kidneys
Enlarged, dark red surface Microscopically, there can be marked glomerular
loops dilation and protein accumulations in the lumen of the tubules (congestive proteinuria).
Accumulations of transudate in the peritoneal cavity – ascites in the pleural space (particularly right)-
effussions in the pericardial space - effusions. Peripheral edema of dependent portions of the
body, especially ankle (pedal) and pretibial edema
Generalized massive edema is called anasarca.
Local venous hyperemia In isolated venous obstruction - some
organs Varied severity, depends on:
The time of appearance of congestion gradually/suddenly
The presence of collaterals, anastomoses Examples
Peripheral venous failure of the legs –valve failure of the veins
Liver ciirhosis –portal hypertension the formation of portosystemic venous
shunts, with the rise in portal venous pressure
veins around and within the rectum (manifest as hemorrhoids),
the cardioesophageal junction (producing esophagogastric varices),
the retroperitoneum -periumbilical and abdominal wall collaterals-caput medusae
Acute venous obstruction + (-) collaterals haemorrhagic necrosis
V. mesenterica –gut V. lienalis V. renalis
Hypostasis
Type of venous hyperemia Where the blood detained in low body
portions In severe ill patients -lungs
Hypostatic pneumonia
HEMORRHAGE Extravasation of blood from vessels into the
extravascular space. 2 types
per rhexin -rupture of a large artery or vein results in severe hemorrhage
due to vascular injury, including trauma, atherosclerosis, or inflammatory or neoplastic erosion of the vessel wall.
per diapedesin (capillary bleeding) chronic congestion, hypoxia-pulmo toxic injury-brain
Hemorrhagic diatheses - clinical disorders with increased tendency to hemorrhage
HEMORRHAGE Hematoma - any accumulation of blood
can be external or can be confined within a tissue can be relatively insignificant (e.g., a bruise) or can involve so much bleeding as to
cause death (e.g., a massive retroperitoneal hematoma resulting from rupture of a dissecting aortic aneurysm
External hemorrhages - into skin, mucous membranes, or serosal surfaces petechiae (1-2mm) –platelets
associated with locally increased intravascular pressure, low platelet counts (thrombocytopenia), defective platelet function, or clotting factor deficiencies
purpura - <1cm (3- to 5-mm) can be associated with many of the same disorders that cause petechiae in addition, can occur with trauma, vascular inflammation (vasculitis), or increased vascular
fragility ecchymoses - larger, >1cm
subcutaneous hematomas (bruises) the hemoglobin (red-blue color) is enzymatically converted into bilirubin (blue-green color) and
eventually into hemosiderin (golden-brown), accounting for the characteristic color changes in a hematoma.
Large accumulations of blood in one or another of the body cavities are called hemo-:
-thorax, -pericardium, -peritoneum, hemarthrosis (in joints).
Acute/chronic
Haemorrhagiae punctatae cerebri
Punctate petechial hemorrhages of the colonic mucosa in
thrombocytopenia Fatal intracerebral hemorrhage
Subcutaneous hematomas (bruises), with characteristic color changes in a hematoma.
HEMORRHAGE The clinical significance of
hemorrhage depends on: the volume and rate of blood loss
rapid removal of as much as 20% of the blood volume or slow losses of even larger amounts may have little impact in healthy adults;
greater losses can cause hemorrhagic (hypovolemic) shock
The site of hemorrhage In subcutaneous tissues/ in the brain
Duration chronic or recurrent external blood loss
(e.g., a peptic ulcer or menstrual bleeding) causes a net loss of iron, frequently culminating in an iron deficiency anemia
HEMOSTASIS AND THROMBOSIS
Normal hemostasis is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels
inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
Thrombosis -the pathologic form of hemostasis it involves blood clot (thrombus) formation in uninjured
vessels or thrombotic occlusion of a vessel after relatively minor injury.
Both hemostasis and thrombosis involve three components
the endotelium the platelets, and the coagulation cascade
ENDOTHELIUM
NORMALLY ANTIPLATELET PROPERTIES ANTICOAGULANT PROPERTIES FIBRINOLYTIC PROPERTIES
IN INJURY PRO-COAGULANT PROPERTIES
It can be activated by infectious agents, hemodynamic factors, plasma
mediators, and cytokines
PLATELETS
Play a critical role in normal hemostasis. When circulating and nonactivated they are membrane-bound
smooth disks expressing several glycoprotein receptors of the integrin family and containing two types of granules:
ALPHA GRANULES Fibrinogen Fibronectin Factor-V, Factor-VIII Platelet factor 4, TGF-beta
DELTA GRANULES (DENSE BODIES) ADP/ATP, Ca+, Histamine, Serotonin, Epineph.
With endothelium, form TISSUE FACTOR
Coagulation Cascade
The third component of the hemostatic process and is a major contributor to thrombosis
An amplifying series of enzymatic conversions; each step in the process proteolytically cleaves an inactive proenzyme into an activated enzyme, eventually culminating in thrombin
The fibrinolytic system
Moderates the size of the ultimate clot plasminogen plasmin
by plasminogen activators - t-PA, Urokinase-like PA (u-PA) , streptokinase
the activity of plasmin is also tightly restricted by: circulating α2-antiplasmin, PAIs (endotelial cells)
Normal Hemostasis A, After vascular injury, local neurohumoral
factors induce a transient vasoconstriction.
B, Platelets adhere (via GpIb receptors) to exposed extracellular matrix (ECM) by binding to von Willebrand factor (vWF) and are activated, undergoing a shape change and granule release.
Released adenosine diphosphate (ADP) and thromboxane A2 (TXA2) lead to further platelet aggregation (via binding of fibrinogen to platelet GpIIb-IIIa receptors), to form the primary hemostatic plug.
C, Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids) results in fibrin polymerization, "cementing" the platelets into a definitive secondary hemostatic plug.
D, Counter-regulatory mechanisms, such as release of t-PA (tissue plasminogen activator, a fibrinolytic product) and thrombomodulin (interfering with the coagulation cascade), limit the hemostatic process to the site of injury.
COAGULATION TESTS
(a)PTT INTRINSIC (HEP Rx) PT (INR) EXTRINSIC (COUM Rx) BLEEDING TIME (PLATS) (2-9min) Platelet count
(150,000-400,000/mm3) Fibrinogen Factor assays
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