Flashcards in Ch4: Hemodynamic Diseases Deck (291):
What is most important cause of morbidity and mortality in Western society?
Cardiovascular disease (35-40% of deaths)
What % of lean body weight is water
2/3 body water is where?
Remainder of body water is where?
What percentage of water is in blood plasma?
Movement of water and solutes is controlled primarily by what?
Opposing effect of vascular hydrostati cpressure and plasma osmotic pressure
What is hydrostatic pressure?
Pressure that pushes things out of capillary into interstitium
What is plasma colloid osmotic pressure?
Pressure pulling things into capillary
Micro edema is what?
Clearing and separation of the extracellular matrix and subtle cell swelling
Edema is commonly seen where? (3)
1. subcutaneous tissue
Subcutaneous edema distribution is usually affected by what?
What is this called
What is it called if in a subcutaneous edema, finger pressure can displace interstitial fluid and leave a depression?
Edema is the result of what?
If edema is in the eyelids it is called?
How much can the weight of lungs change in pulmonary edema?
Edema in the brain can present in what two ways?
Localized or generalized
Five pathophysiologic categories of edema
1. Increased hydrostatic prssure
2. Reduced plasma osmotic pressure
3. Lymphatic obstruction
4. Sodium retention
Increased hydrostatic pressure results from what?
Impaired venous return
Impaired venous return can be caused by what? (5)
2. Constrictive pericarditis
4. Venous obstruction or compression
5. Arteriolar dilation
Reduced plasma osmotic pressure is known as what?
What can cause hypoproteinemia? 4
4. Protein-losing gastroenteropathy
Lymphatic obstruction can be of what 4 types?
Two causes of sodium retention?
Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium
What can cause increased tubular reabsorption of sodium? 2
Increased renin-angiotensin-aldosterone secretion
Three inflammations that can cause edema?
Edema simply means?
abnormal Increase in interstitial fluid
If edema is in chest it is called?
If edema is in heart, it is called?
If edema is in the peritoneum, it is called?
What is anasarca?
severe generalized edema with widespread subcutaneous tissue swelling
What is transudate?
What is exudate?
Regional increases in hydrostatic pressure can result from what?
Focal impairment such as DVT
Generalized increases in venous pressure with systemic edema is the result of what?
Main cause of reduced plasma osmotic pressure?
Albumin not synthesized in correct amount or lost from circulation
3 causes of albumin discrepancies?
Nephrotic syndrome (generalized edema)
Severe liver disease
What does reduced plasma osmotic pressure lead to?
Decreased renal perfusion
Sal retention occurs when?
Renal function is compromised (CHF)
Primary retention of water is produced by what?
Release of ADH
Inappropriate releases of ADH can be the result of what? (2)
2. pituitary disorders
What does inappropriate release of ADH lead to?
2. Cerebral edema
What will happen to patient with hyponatremia if you correct salt balance too quickly?
Patient will get central pontine myelinolysis which causes damage to myelin sheath in pons
Impaired lymphatic drainage leads to what?
Causes of lymphedema? (5)
chronic inflammation with fibrosis,
invasive malignant tumors,
parasitic lymphatic obstructure is called what?
Results in what disease?
Severe edema of the upper extremity may hamper what procedure?
Removal or irradation of breast and lymph nodes in patients with breast cancer
Carcinoma of the breast that obstructs lymphatic presents as what?
What does subcutaneous tissue edema signal? (2)
1. Cardiac disease
2. Renal disease
Subcutaneous edema can impair what? 2
1. Impair wound healing
2. Clearance of infection
When is pulmonary edema most frequently seen?
1. LV failure
2. renal failure
4. pulmonary inflammation/ifection
How serious is brain edema?
What is hyperemia?
active process of ↑ blood flow due to arteriolar dilation
What is congestion?
passive process resulting from reduced outflow of blood from a tissue
Cause of local congestion?
Isolated venous obstruction
Cause of systemic congestion?
Tissue color in congestion?
What does congestion lead to?
Chronic passive congestion leads to what?
Acute pulmonary hyperemia results from what?
engorged alveolar capillaries often with alveolar septal edema and focal intra-alveolar hemorrhage
Pulmonary congestion results from what?
thickened & fibrotic septa
Main sign of chronic pulmonary congestion
alveoli often contain numerous hemosiderin-laden macrophages (called heart failure cells)
What happens in hepatic hyperemia?
central vein and sinusoids are distended; centrilobular ischemia
What happens in hepatic congestion?
centrilobular regions grossly red-brown and slightly depressed because of cell death (nutmeg liver)
Microscopically: centrilobular hemorrhage, hemosiderin-laden macrophages, and degeneration of the hepatocytes
Centriolbular area is prone to undergo necrosis (distal end of the blood supply)
What is hemorrhage?
extravasation of blood into extravascular spaces
What is a hematoma
What is petechiae?
1- to 2-mm hemorrhages into skin, mucous membranes, or serosal surfaces
Cause of petechiae? 3
increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function
What is purpura?
: > 3mm hemorrhages
Causes of purpura? 6
increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function
Increased vascular fragility
What are ecchymoses?
larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises)
What causes the color changes of bruises?
hemoglobin (red-blue color) → bilirubin (blue-green color) → hemosiderin (gold-brown color)
What are some of the special names for accumulation of blood in a cavity?
hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
Patients with extensive bleeding can develop what?
massive breakdown of RBCs and Hgb
Up to what rate will healthy adults not notice hemorrhage?
Rapid loss of up to 20% of the blood volume or slow losses of even larger amounts
If you go over the 20% threshold of blood lost, what will the body go into?
hemorrhagic (hypovolemic) shock
Is site important for hemorrhage?
Yes, for example if hemorrhage is in head, you have no margin. If an abdomen, you could probably lose quite a bit
Chronic or recurrent external blood loss leads to what?
What is named what?
Net loss in iron
Iron deficiency anemia
Physiologic thrombosis is called what?
Pathologic clot is called what?
Three main components of thrombosis?
1. vascular wall
3. coagulation cascade
Injury to the endothelium results in what?
What regulates this? (2)
1. Transient arteriolar vasoconstriction
reflex neurogenic mechanisms and endothelin
Endothelial injury exposes what?
Highly thromobogenic subendothelial ECM
What is primary hemostasis?
Platelets adhere to wound site, become activated, aggregating to form a hemostatic plug
When tissue factor is endothelium is exposed, what does it do?
Activates coagulation cascade
Activation of thrombin allows it to do what?
converts soluble fibrinogen to insoluble fibrin (secondary hemostasis)
What is secondary hemostasis?
Polymerized fibrin and platelet aggregates form a solid, permanent plug
At the same time, what is going on during secondary hemostasis
Counter-regulatory mechanisms are set into motion to limit the hemostatic plug to the site of injury
How does thrombin act contradictory?
1. Activates fibrinogen to fibrin to cross link clots
2. Binds to thrombomodulin to inhibit cascade
What determines whether thrombus formation, propagation, or dissolution occurs?
1. Anti-thrombotic activities of endothelium
2. Pro-thrombotic activities of endothelium
What does the endothelium normally exhibit?
Anti-thrombotic activities (antiplatelet, anticoagulant, fibrinolytic properties)
What does the endothelium exhibit during injury/activation?
3 anti-platelet effects of endlthelium?
1. Intact endothelium keeps platelets off the subendothelial ECM
2. PGI2 and NO produced by endothelial cell impede platelet adhesion
3. Also elaborate adenosine diphosphatase (degrades ADP) and further inhibits platelet aggregation
4 anti-coagulant effects of endothelium?
1. Membrane heparin-like molecules (interact with ATIII to inactivate thrombin)
2. Thrombomodulin: a thrombin receptor (converts thrombin to an anticoagulant → activates protein C)
Protein C inactivates factors Va and VIIIa
3. Protein S (cofactor for Protein C)
4. Tissue factor pathway inhibitor (TFPI) Inhibits VIIa and Xa
Fibrinolytic effect of endothelium?
Synthesis of tissue-type plasminogen activator (t-PA), promoting fibrinolysis
Platelet prothrombotic properties of endlthelium?
Produce vWF (essential cofactor for platelet binding to matrix elements)
Procoagulant effects of endothelium? 2
1. Synthesis of tissue factor, major activator of extrinsic cascade
2. Augment the catalytic function of activated coagulation factors IXa and Xa
Antifibrinolytic effects of endothelium?
Secrete inhibitors of plasminogen activator (PAIs)
Limits fibrinolysis and tend to favor thrombosis
Platelets are what type of cells?
What are they shed from?
Disc-shaped, anucleate cell fragments
Shed from megakaryocytes in the bone marrow
Function of platelets depends on what? (3)
Two types of cytoplasmic platelet granules?
Alpha granules have what special adhesion molecule?
Also contain what? (7)
3. Factor V
4. Factor VIII
5. Platelet factor 4
What do dense granules contain? 6
3. Ionized Ca
After vascular injury, what do platelets encounter?
ECM constituents collagen and vWF
Upon coming into contact with collagen and vWF, what do platelets do? 3
Adhesion and shape change
Platelet adhesion is mediated by what?
Bridge between the platelet surface receptor (glycoprotein Ib—GpIB) and exposed collagen
Platelet secretion involves what molecules?
alpha and dense after adhesion
Release of platelet dense granules is important why? 2
1. calcium is required for the coagulation cascade
2. ADP is a potent activator of platelet aggregation
Aggregation of platelets requires what? 4
What are steps of txA2 function? 2
Amplify platelet aggregation
Formation of primary hemostatic plug
How does thrombin activation stabilize the plug?
Binding to a protease-activated receptor on the platelet membrane → platelet contraction --> irreversibly fused mass of platelets
Most important component of platelet aggregation is what?
How does platelet bind to fibrinogen?
1. activation by adp
2. conformation change in platelet GpIIb-IIIa receptors
3. Binding to brinogen
Deficiency in GpIIb-IIIa complex results in what?
Deficiency in GpIb results in what?
Deficiency in vWF leads to what?
Von Willebrand disease
What does Clopidogrel do?
blocks platelet by blocking ADP binding
Synthetic antagonists or monoclonal antibodies have what effect on platelets?
bind to the GpIIb-IIIa receptors
Effect on aspirin on platelets?
permanently blocks platelet TxA2 synthesis; endothelial PGI2 production is also inhibited by aspirin
How do cells overcome aspirin blockade of cascade?
resynthesize active cyclooxygenase
Nitric oxide effect on platelets?
acts as a vasodilator and inhibitor of platelet aggregation
What is intrinsic coagulation pathway?
What is extrinsic coagulation pathway?
What is the common coagulation pathway?
What is the coagulation cascade?
Amplifying series of enzymatic conversions; each step proteolytically cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation
What is the most important coagulation factor?
Explain the changes thrombin makes on fibrinogen
fibrinogen → fibrin monomers → insoluble gel → secondary hemostatic plug
What stabilizes and cross links fibrin polymers?
What activates this?
Each reaciton in coagulation pathway results from what?
Assembly of a complex of enzyme, substrate, cofactor
What is the enzyme in coagulation reactions?
Activated coagulation factor
What is the substrate in coagulation reactions?
Proenzyme form of coagulation factor
What is the cofactor in coagulation reactions?
Where does the coagulation reaction take place?
What holds it all together?
Factors 2, 7, 9, and 10 binding to calcium requires what as cofactor?
What antagonizses factors 2, 7, 9, 10 as an anti-coagulant?
Extrinsic and intrinsic pathways converge on activation of what?
Why is the extrinsic pathway named so?
it required the addition of an exogenous trigger
What is the most physiologically relevant pathway for coagulation when vascular damage has been ocurred?
What activates extrinsic pathway?
What does prothrombin (PT) time measure?
measures VII, X, II, V, and fibrinogen
What measures the intrinsic pathway?
Partial thromboplastin time (PTT) screens for the function of the proteins (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)
Thrombin exerts what type of effects?
How does thrombin modulate cellular activities?
Protease-activated receptors (PARs)
What type of activities do the PAR's through thrombin work? 3
I1. nduces platelet aggregation and TxA2 production
2. Activates ECs to express adhesion molecules, and a variety of fibrinolytic (t-PA), vasoactive (NO, PGI2), and cytokine mediators (e.g., PDGF)
3. Directly activates leukocytes
Coagulation cascade must be restricted to where?
Only site of vascular injury
Antithrombins are activated how?
binding to heparin-like molecules on endothelial cells
Antithrombins act how?
inhibit the activity of thrombin and other serine proteases, including factors IXa, Xa, XIa, and XIIa
How is heparin used?
What are proteins C and S dependent on?
What is action of proteins C and S?
Inactivate factors Va and VIIIa
What is the protein produced by endothelium that inactivates tissue factor-factor VIIa complexes
Activation of clotting cascade sets what into motion?
How does the fibrinolytic cascade limit size of clot?
breaks down fibrin and interferes with its polymerization
Generation of plasmin results in what?
fibrin split products (FSPs) can also act as weak anticoagulants
Elevated levels of FSP's can be used in what?
diagnosing abnormal thrombotic states (DIC, DVT, PE)
The fibrinolytic system has what main reaction?
Enzymatic conversion of inactive precursor plasminogen to plasmin
Two main types of plasminogen activators?
Tissue-type PA (t-PA) synthesized by endothelium
Urokinase-like PA (u-PA)
Main bacterial plasminogen activator?
Streptokinase (bacterial enzyme
Free plasmin is rapidly inactivated by what?
Endothelial cells also release what to inhibit plasminogen activation?
plasminogen activator inhibitor (PAI) which inhibits t-PA
Abnormalities that lead to thrombus formation are together known as what?
What are the 3 components of Virchow's triad
Stasis or turbulent blood flow
Hypercoagulability of the blood
Endothelial injury is important factor in what?
heart or the arterial circulation (normally high flow rates might otherwise impede clotting)
Does the endothelium need to be physically disrupted to contribute to thrombosis?
Abnormality in the balance of prothrombotic and antithrombotic activities of endothelium can influence local clotting events
What can induce endothelial dysfunction? (6)
Turbulent blood flow
Metabolic abnormalities (homocystinemia, hypercholesterolemia)
Toxins (cigarette smoke)
Turbulence leads to what?
endothelial injury or dysfunction
Can form countercurrents and local areas of stasis
What is main contributor in development of venous thrombi?
Normal blood flow is described how?
(platelets and blood cellular components flow centrally separated from the endothelium by slower moving plasma)
Stasis promotes activation of what?
Flow-induced changes in endothelial cell gene expression
Stasis disrupts flow and brings what into contact with endothelium?
What does stasis prevent?
dilution of activated clotting factors
Atherosclerotic plaques are involved in thrombosis how?
expose subendothelial ECM and cause turbulence
Aneurysms are involved in thrombosis how?
Acute MI's are involved in thrombosis how?
areas of noncontractile myocardium and sometimes cardiac aneurysms→ formation of cardiac mural thrombi
Rheumatic mitral valve stenosis is involved in thrombosis how?
left atrial dilation
Hypoviscosity is involved in thrombosis how?
increases resistance to flow and causes small vessel stasis
Sickle cell anemia is involved in thrombosis how?
vascular occlusions→ stasis → thrombosis
What will hypercoagulability contribute to?
Primary hypercoagulability is due to what?
Point mutations in the factor V gene and prothrombin gene are the most common
Secondary hypercoagulability is due to what?
Factor V Leiden is found in what population
2% to 15% of Caucasians carry a single nucleotide mutation in factor V
Mutation in Factor V Leiden results in what?
factor V resistant to cleavage by protein C
Prothrombin mutation results in what?
Increased levels of prothrombin with an almost threefold increased risk of venous thromboses
Elevated levels of homocysteine contribute to what?
Contribute to arterial and venous thrombosis as well as the development of atherosclerosis
Why do mild elevated levels of homocysteine occur?
Variant form of 5,10-methylenetetrahydrofolate reductase
Markedly elevated homocysteine levels can be caused by what?
inherited deficiency of cystathione β-synthetase
What can reduce plasma homocysteine concentration?
Folic acid, pyridoxine, and/or vitamin B12
Rare inherited causes of increase risk in thrombosis are due to deficiencies in what?
Some causes of acquired thrombophilia
1. Oral contraceptive use
2. Hyperestrogenic state of pregnancy
3. Dissemianted cancers
4. Reduced endothelial PGI2 in age
Why do oral contraceptive use or hyperestrogenic state of pregnancy cause thrombosis? 2
increased hepatic synthesis of coagulation factors and reduced anticoagulant synthesis
What is heparin-induced thrombocytopenia syndrome?
After adminstration of unfractionated heparin, there is Induction of the appearance of antibodies that recognize complexes of heparin and platelet factor 4
Result of heparin-induced thrombocytopenia syndrome?
1. platelet aggregation
2. Platelet activation
3. platelet consumption
What will alleviate heparin-induced thrombocytopenia syndrome
Low-molecular weight heparin
Antiphospholipid syndrome is known as what?
lupus anticoagulant syndrome
How does antiphopholipid syndrome present clinically? 4
Recurrent venous or arterial thrombi
Cardiac valvular vegetations
Antiphospholipid syndrome is mediated by what?
binding of antibodies to epitopes on plasma proteins that are induced by phospholipids
What does antiphospholipid syndrome present as on serologic test?
What is secondary antiphospholipid syndrome?
individuals with a well-defined autoimmune disease
What is primary antiphospholipid syndrome?
patients with a hypercoagulable state with no evidence of other autoimmune disorders
Thrombi can develop where in the CV system?
Size and shape of thrombi depend on what?
site of origin and cause
Thrombi are attached to what?
Underlying vascular surface
Arterial thrombi grow what direction?
Retrograde (toward heart)
Venous thrombi grow what way?
Direction of blood flow (toward heart)
What are Lines of Zahn
pale platelet and fibrin deposits alternating with darker red cell–rich layers
What do lines of Zahn signify?
thrombus formed in flowing blood
Mural thrombi occur where?
heart chambers or in the aortic lumen
What promotes cardiac mural thrombi? 2
Abnormal mycardial contraction (arrhythmia, MI)
Endomyocardial injury (myocarditis)
Arterial thrombi has what characteristics? 3
2. Superimposed on a ruptured atherosclerotic plaque
3. Seen with other vascular injuries
Common sites of arterial thrombi?
Coronary, cerebral, femoral arteries
Venous thrombosis has what characteristics? 2
1. Occlusive with thrombus forming a long cast of lumen
2. More enmeshed red cells and few platelets
Thrombi of veins normally occur where?
Where else (4)
1. upper extremities
2. Perioprostatic plexus
4. periuterine veins
Posmortem clots appear how? 3
Gelatinous with a dark red dependent portion
Yellow upper portion “chicken fat”
Not attached to the underlying wall
Thrombi on heart valves are known as?
What is infective endocarditis?
bacteria or fungi adhering to previously damaged valves or directly causing valve damage; formation of large thrombotic masses
What is nonbacterial thrombotic endocarditis?
sterile vegetations on noninfected valves in persons with hypercoagulable states
What is sterile, verrucous endocarditis/Libman-Sacks endocarditis?
Seen in setting of SLE
What is propagation?
thrombi accumulate additional platelets and fibrin
What is embolization?
thrombi dislodge and travel to other sites in the vasculature
What is dissolution?
fibrinolysis with rapid shrinkage and disappearance of recent thrombi
What is organization and recanalization?
ingrowth of endothelial cells, smooth muscle cells, and fibroblasts; capillary channels eventually form that re-establish the continuity of the original lumen
Where do most venous thrombosis (phlebothrombosis) occur?
Superficial or deep veins of leg
Characteristics of superficial venous thrombosis?
local congestion, swelling, pain, and tenderness; rarely embolize
Characteristics of DVT?
in the larger leg veins
More often embolize to the lungs and give rise to pulmonary infarction
Can cause local pain and edema
DVTs are asymptomatic in approximately 50% of affected individuals
Lower extremeties DVT's are associated with what?
Common predisposing factors?
Bed rest and immobilization
Congestive heart failure
Trauma, surgery, and burns
What is trousseau syndrome?
Due to what?
Tumor-associated inflammation and coagulation factors (tissue factor, factor VIII) and procoagulants (e.g., mucin) released from tumor cells all contribute to the increased risk of thromboembolism in disseminated cancers
Major cause of arterial thromboses?
Can cardiac and aortic mural thrombi embolize peripherally?
Targets of cardiac and aortic mural thrombi?
Brain, kidneys, and spleen are particularly likely targets because of their rich blood supply
Disseminated intravascular coagulation is seen when?
obstetric complications to advanced malignancies
What happens in Disseminated intravascular coagulation?
Sudden or insidious onset of widespread fibrin thrombi in the microcirculation
Result of Disseminated intravascular coagulation?
Can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart, and kidneys
Widespread microvascular thrombosis results in platelet and coagulation protein consumption and at the same time the fibrinolytic mechanisms are activated
DIC is a complication of any condition associated with what?
widespread activation of thrombin
What is an embolism?
Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
Almost all emboli represent what?
some part of a dislodged thrombus (thromboembolism)
Emboli will inevitably lodge where?
in vessel too small to permit further passage (causing partial or completely vascular occlusion)
A major consequence of an embolism is what?
A major consequence of embolism is what?
Ischemic necrosis (infarction)
Pulmonary embolism usually results from what?
Occlusion of main pulmonary artery bifurcation is what?
What is a pardoxical embolism?
embolus can pass through an interatrial or interventricular defect and gain access to the systemic circulation
Do most PE's have symptoms?
Nope, too small
If more than 60% of pulmonary circulation is obstructed, what will happen?
Sudden death, right heart failure, or CV collapse
Embolic obstruction of medium-sized pulmonary arteries result in what?
pulmonary hemorrhage but not usually infarction
Embolic obstruction of small end-arteriolar pulmonary branches result in what?
hemorrhage or infarction
Multiple emboli in PE overtime results in what?
pulmonary hypertension and right ventricular failure
What is systemic thromboembolism?
Emboli in the arterial circulation
Most arterial emboli arise from where?
intracardiac mural thrombi
2/3 of arterial emboli are associated with what?
left ventricular wall infarcts
1/4 of arterial emboli are associated with what?
left atrial dilation and fibrillation
Remainder of arterial emboli arise from what?
thrombi on ulcerated atherosclerotic plaques, aortic aneurysms, or fragmentation of a valvular vegetation, or paradoxical emboli
Sites for arterial emboli to lodge? and their percentage
Lower extremities: 75%
Intestines, kidneys, spleen
What is a fat or marrow emboli?
Microscopic fat globules—with or without associated hematopoietic marrow elements—can be found in the circulation and in the pulmonary vasculature
When are fat/marrow emboli seen?
Fractures of long bones
Vigorous cardiopulmonary resuscitation
Fat Embolism Syndrome is what?
Term applied to the minority of patients who become symptomatic
Causes of fat embolism syndrome? 3
Anemia and thrombocytopenia
Presentatin of symptoms in fat embolism syndrome?
1. After 1-3 days, sudden onset of tachypnea, dyspnea, and tachycardia
2. Diffuse petechial rash (thrombocytopenia)
What is an air embolism?
Gas bubbles can coalesce to form frothy masses that obstruct vascular flow
How much air is required to have a clinical effect in pulmonary circulation?
more than 100 cc of air
When can an air embolism occur? (2)
obstetric or laparoscopic procedures or because of chest wall injury
What is decompression sickness due to?
Sudden decreases in atmospheric pressure and Gas (particularly nitrogen) dissolves in the blood and tissues
What are the bends?
– rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints
What are the chokes?
respiratory distress where gas bubbles in the lungs cause edema, hemorrhage, and focal atelectasis or emphysema
Treatment for decompression sickness?
Caisson disease is a chronic form of what?
Caisson disease is what?
Gas emboli in bones
Ischemic necrosis of femoral head, tibia and humerus
Why is amniotic fluid embolism so serious?
80% mortality rate and fifth most common cause of maternal mortality worldwide
What happens in amniotic fluid embolism?
infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of the uterine veins
Result of amniotic fluid embolisM?
severe dyspnea, cyanosis, and shock followed by neurologic impairment
Pulmonary edema and DIC
Findings in amniotic fluid embolism?
Presence of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or GI tract in the maternal microvasculature
marked pulmonary edema, diffuse alveolar damage, and presence of fibrin thrombi in many vascular beds due to DIC
What is ischemic necrosis?
Occlusion of arterial supply or venous drainage
Nearly all infarcts result from what?
thrombotic or embolic arterial occlusions
Infarction is classified according to what?
Color, presence of infection
3 types of infarctions
Red or hemorrhagic infarcts
White or anemic infarcts
Septic or bland
Red infarcts are most commonly caused where?
Characteristics of places where red infarcts occur?
Venous occlusions (ovary)
Loose tissues when blood can collect in the infarcted zone (lung)
Tissues with dual circulation (lung, small intestine)
Tissues previously congested by sluggish venous outflow
Flow is re-established to a site of previous arterial occlusion and necrosis
When do white infarcts occur?
arterial occlusion in solid organs with end-arterial circulation (heart, spleen, kidney)
Tissue density has what effect on white infarct
limits the seepage of blood from adjoining capillary beds into the necrotic area
Wedge-shaped infarct is what?
Occluded vessel at the apex and the periphery of the organ forming the base
Dominant histologic characteristic of infarct is what?
ischemic coagulative necrosis
Most infarcts are replaced by what?
In brain how do infarcts present?
Septic infarcts may lead to what?
Factors that influence development of an infarct? 4
1. Nature of vascular supply
2. Rate of occlusion development
3. Vulnerability to hypoxia
4. Oxygen content of blood
What is common pathway for potentially lethal clinical events?
What can cause shock? (5)
Severe hemorrhage, extensive trauma or burns, large MI, massive PE, microbial sepsis
Shock is characterized by what?
Due to what? (2)
Which results in what?
1. Reduced CO
2. Reduced effective circulating blood volume
1. Impaired tissue perfusion
2. Cellular hypoxia
Three main categories of shock
Cardiogenic shock is due to what?
low CO due to myocardial pump failure
What can cause cardiogenic shock?
MI, ventricular arrhythmias, external compression (cardiac tamponade), outflow obstruction (PE)
What is hypovolemic shock?
Due to what? 2
low CO due to loss of blood or plasma volume
Hemorrhage, severe burns