• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/89

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

89 Cards in this Set

  • Front
  • Back
What is hemorrhage?
1) The escape of blood from the vasculature into surrounding tissues, a hollow organ or body cavity, or to the outside.
2) Is most often caused by trauma.
List four types of hemorrhage.
1) Hematoma
2) Hemothorax, hemopericardium, hemoperitoneum, and hemarthrosis.
3) Petechial hemorrhages, petechiae, or purpura.
4) Ecchymosis
What is a hematoma?
Localized hemorrhage within a tissue or organ.
Where do hemothorax, hemopericardium, hemoperitoneum and hemarthrosis hemorrhage?
Into the pleural cavity, pericardial sac, peritoneal cavity, or a synovial space respectively.
Where do petechial hemorrhages, petechiae, or purpura hemorrhage?
Small punctate hemorrhages in the skin, mucous membranes, or serosal surfaces.
Where can you find eccyhmosis?
Diffuse hemorrhage, usually in skin and subcutaneous tissue.
What is hyperemia?
Localized increase in the volume of blood in capillaries and small vessels.
What is active hyperemia?
Results from localized arteriolar dilation (blushing, inflammation)
What is passive congestion/passive hyperemia?
Results from obstructed venous return or increased back pressure from CHF.
When does acute passive congestion occur?
Occurs in shock, acute inflammation, or sudden right heart failure.
Where does chronic passive congestion occur?
Lung and Liver
Describe chronic passive congestion of the lung.
1) Most often caused by left heart failure or mitral stenosis.
2) Congestion and distention of alveolar capillaries lead to capillary rupture and passage of red cells into alveoli.
3) Phagocytosis and degradation of red cells result in intra-alveolar hemosiderin-laden macrophages called heart-failure cells.
4) Long-standing congestion, fibrosis of interstitium and hemosiderin deposition result in brown induration of the lung.
Describe chronic passive congestion of the liver.
1) Most often caused by right heart failure.
2) Nutmeg liver may appear; this speckled nutmeg appearance on cross section is produced by a combination of dilated, congested central veins and the surrounding brownish-yellow, often fatty, liver cells.
What is an infarction?
Necrosis resulting from ischemia caused by obstruction of the blood supply. The necrotic tissue is referred to an infarct.
Describe an anemic infarct.
1) White or pale infarcts
2) Usually caused by arterial occlusions in the heart, spleen, and kidney.
Describe a hemorrhagic infarct.
1) Red infarcts, in which red cells ooze into the necrotic area.
2) Occur characteristically in the lung and gastrointestinal tract as the result of arterial occlusion. These sites are loose, well-vascularized tissues with redundant arterial blood supplies and hemorrhage into the infarct occurs from the nonobstructed portion of the vasculature.
3) Can also be caused by venous occlusion. This is an important contribution to infarcts associated with volvulus, incarcerated hernias, an port-operative adhesions.
What is Thrombosis?
1) Intravascular coagulation of blood, often causing significant interruption of blood flow.
2) Pathologically predisposed by many conditions, including venous stasis, usually from immobilization; CHF; polycythemia; sickle cell dz.;visceral malignancies; and the use of oral contraceptives, esp. in assoc. with cigarette smoking.
What is thrombogenesis?
Results from the interaction of platelets, damaged endothelial cells, and the coagulation cascade.
Describe platelet functions.
1) Maintain the physical integrity of the vascular endothelium.
2) Participate in endothelial repair through the contribution of platelet-derived growth factor (PDGF).
3) Form platelet plugs
4) Promote the coagulation cascade through the platelet phospholipid complex.
What is involved in platelet adhesion?
1) Vessel injury exposes subendothelial collagen, leading to platelet adhesion
2) Interaction of specific platelet-surface glycoprotein receptors and subendothelial collagen is mediated by von Willebrand factor.
What is the platelet release reaction?
Soon after adhesion, platelets release adenosine diphosphate (ADP), histamine, serotonin, PDGF, and other patelet granule constituents.
How are platelets involved in the activation of coagulation cascade?
Conformational change in the platelet membrane makes the platelet phospholipid complex available, thus contributing to the activation of the coagulation cascade, leading to the formation of thrombin.
How are platelets involved in arachidonic acid metabolism?
1) Arachidonic acid, provided by activation of platelet membrane phospholipase, proceeds through the cyclooxygenase pathway to the production of thromboxane A2 (TxA2).
2) Platelet TxA2 is a potent vasoconstrictor adn platelet aggregant.
3) The inhibition of cyclooxygenase by low-dose aspirin is the basis of aspirin therapy for prevention of thrombotic disease.
What is involved in platelet aggregation?
1) Platelets stick to each other.
2) Additoinal platelets are recruited from the circulation to produce the initial hemostatic platelet plug.
What agonists promote platelet aggregation?
1) ADP
2) Thrombin
3) TxA2
4) Collagen
5) Epinephrine
6) Platelet activating factor
How is the platelet plug stabilized?
1) Fibrinogen bridges bind the aggregate platelets together.
2) The platelet mass is stabilized by fibrin.
What limits platelet plug formation?
1) Prostacyclin (PGI2), another product of the cyclooxygenase pathway, is synthesized by endothelial cells.
2) Endothelial PGI2 is antagonistic to platelet TxA2 and limits further platelet aggregation.
3) Fibrin degradation products are also inhibitors of platelet aggregation.
Describe endothelial cells.
1) Resistant to the thrombogenic influence of platelets and coagulation proteins.
2) Intact endothelial cells act to modulate several aspects of hemostasis and oppose coagulation after injury by thromboresistance.
What do endothelial cells do?
1) Produce heparin-like molecules ( proteoglycans that activate antithrombin III), which neutralizes thrombin and other coagulation factors, including IXa and Xa
2) Secrete plasminogen activators, such as TPA
3) Degrade ADP
4) Take up, inactivate, and clear thrombin.
5) Synthesize thrombomodulin
6) Synthesize protein S, a cofactor for APC
7) Synthesize and release PGI2
8) Synthesize and release NO (similar actions to PGI2)
What does thrombomodulin do?
1) A cell surface protein that binds thrombin and converts it to an activator of protein C, a vitamin K-dependent plasma protein.
2) Activated protein C (APC) cleaves factors Va and VIIIa, thus inhibiting coagulation.
What are the steps in the extrinsic pathway of coagulation?
1) Initiated by tissue factor
2) TF activates factor VII and forms a tissue factor-factor VIIa complex.
3) Complex initiates coagulation through the activation of factor X (and also factor IX)
4) Factor Xa converts prothrombin to thrombin.
5) Factor Va is a cofactor required in step 4.
6) Thrombin converts fibrinogen to fibrin.
How is the fibrin clot formed?
Prothrombin-mediated cleavage of fibrinogen results in a fibrin monomer, which is polymerized and stabilized by factor XIII.
What is the action of tissue factor-factor VIIa complex limited by?
tissue factor pathway inhibitor
How is the extrinsic pathway clinically evaluated?
Prothrombin time (PT)
What does prothrombin time test?
factors: II, V, VII, X and fibrinogen
What clotting factors are involved in the intrinsic pathway?
all except VII and XIII
What is contact activation in the intrinsic pathway and why is it important?
1) Interactions of the so-called contact factors: factor XII (Hageman), prekallikrein, and high-molecular-weight kininogen (HMWK), and factor XI.
2) It's important in in-vitro clotting in glass containers and in laboratory testing, but it's physiologic role has been questioned because a deficiency of the contact factors is not associated with abnormal bleeding.
How is the intrinsic pathway initiated?
1) Probably by the TF-factor VIIa complex (from extrinsic), activating factor IX.
2) Factor IXa leads to the conversion of factor X (catalyzed by factor VIIIa).
How is the intrinsic pathway activated?
By the platelet phospholipid complex, which becomes available through conformational changes in the platelet membrane.
How does thrombin work within the intrinsic pathway?
It's production further stimulates the pathway by the activation of factor XI and cofactors V and VIII.
How do you evaluate the intrinsic pathway clinically?
Partial Thromboplastin Time (PTT).
What does the PTT measure?
factors II, V, VIII, IX, X, XI, XII and fibrinogen.
What is fibrinolysis?
1) concurrent with thrombogenesis and modulates coagulation.
2) Restores blood flow in vessels occluded by a thrombus and facilitates healing after inflammation and injury.
How does fibrinolysis work?
1) Plasminogen is converted by proteolysis to plasmin, the most important fibrinolytic protease.
2) Plasmin splits fibrin.
3) A classic teaching has been that factor XII activation links the fibrinolytic system, coagulation system, complement system, and kinin system.
Describe two types of thrombotic disorders.
1) Antithrombotic (hemorrhagic), leading to pathologic bleeding states such as hemophilia, Christmas disease, and von Willebrand disease.
2) Prothrombotic, leading to hypercoagulability with pathologic thrombosis.
Describe hereditary thrombophilia.
1) Prothrombotic familial syndrome occuring most often in adolescents or young women.
2) Characterized by recurrent venous thrombosis and thromboembolism.
3) Can be caused by deficiency of a number of antithrombotic proteins, including antithrombin III, protein C, and protein S.
List four types of hereditary thrombophilia.
1) Factor V Leiden
2) Prothrombin 20210A transition
3) Methylene tetrahydrofolate reductase mutation (MTHFR-C677T).
What is factor V Leiden?
1) Most frequent cause of hereditary thrombophilia.
2) An abnormal factor V protein with a specific mutation that alters the cleavage site targeted by APC. The mutation prevents the cleavage and inactivation of the mutant factor Va by APC, a phenomenon referred to as hereditary resistance to activated protein C.
What is Methylene tetrahydrofolate reductase mutation (MTHFR-C677T)?
1) Results in a moderate increase in serum homocysteine, which is associated with both arterial and venous thrombosis. The homocysteine can be reduced by dietary supplementation with folic acid and vitamin B6 and B12.
2) Also associated with an increased risk of neural tube defects and possibly a number of diverse neoplasms.
What happens with an increased level of factor VIII, IX, XI or fibrinogen?
Associated with increased venous thrombosis.
What is antiphospholipid antibody syndrome?
1) Prothrombotic disorder characterized by autoantibodies directed against a number of protein antigens complexed to phospholipids.
2) Characterized by recurrent venous and arterial thromboembolism, fetal loss, thrombocytopenia, and a variety of neurologic manifestations.
How is Antiphospholipid antibody syndrome most often diagnosed?
1) Incidental finding of a prolonged PTT.
2) This is a paradoxical abnormality, because a prolonged PTT is usually considered to be an indicator of antithrombotic syndromes.
3) This is thought to be an in vitro artifact caused by interaction of the antiphospholipid antibodies with the phospholipid reagent used in the PTT test.
What autoimmune disease is antiphospholipid antibody syndrome associated with?
1) SLE
2) For this reason, an antiphospholipid antibody that prolongs the PTT is sometimes referred to as the lupus anticoagulant.
3) Another antiphospholiped antibody associated with SLE is the anticardiolipin antibody, which can cause a false-positive serologic test for syphilis.
What is Disseminated intravascular coagulation (DIC)?
Both a prothrombotic and antithrombotic disorder characterized by widespread thrombosis and hemorrhage resulting form the consumption of platelets and coagulation factors.
Describe the morphological characteristics of arterial thrombi.
1) Are formed in areas of active blood flow.
2) When mature, demonstrate alternate dark gray layers of platelets interspersed with lighter layers of fibrin. This layering results in the lines of Zahn.
3) Eventually liquefy and disappear or are organized with fibrous tissue formation. Recanalization, new blood vessel formation within a thrombus, restores blood flow.
Describe the morphological characteristics of venous thrombi.
1) Are formed in areas of less active blood flow, most often in the veins of the lower extremities and in the periprostatic or other pelvic veins.
2) Are predisposed by venous stasis, with a high incidence occuring in hospitalized patients on bed rest.
3) Are dark red with a higher concentration of red cells than arterial thrombi. Lines of Zahn are not prominent or are absent.
4) Is often associated with concurrent venous inflammatory changes. Inflammation of veins with thrombus formation is referred to as thrombophlebitis.
Describe postmortem clots.
1) Appear soon after death and are not true thrombi.
2) In contrast to true thrombi, are not attached to the vessel wall.
3) Settling of red cells results in a two-layered appearance: currant jelly appearance in the red cell-rich lower layer and a chicken fat appearance in the cell-poor upper layer.
What is an embolism?
The passage and eventual trapping within the vasculature of any of a wide variety of mass objects.
What are three types of thromboembolism?
1) Pulmonary emboli
2) Arterial emboli
3) Paradoxical emboli
Describe Pulmonary emboli.
1) Important cause of sudden death, usually occurring in immobilized postoperative patients and in those with CHF.
2) Immobilization leads to venous thrombosis in the lower extremities. Portions of the friable thrombus break away, travel through the venous circulation, and lodge in branches of the pulmonary artery.
3) PE vary in size from saddle emboli obstructing the bifurcation of the pulmonary artery, which can produce sudden death, to less clinically significant small emboli. Emboli of intermediate size can cause pulmonary hypertension and acute right ventricular failure.
4) Obstruction of the pulmonary artery leads to pulmonary infarction, a term often used interchangeably with pulmonary embolism. Hemorrhagic pulmonary infarcts result. These are characteristically wedge-shaped and located just beneath the pleura.
Describe Arterial emboli.
Usually arise form a mural thrombus, a thrombus that adheres to one wall of a heart chamber or major artery.
Describe the sites of origin of arterial emboli.
1) In the LA are associated especially with mitral stenosis with atrial fibrillation.
2) In the LV are caused by MI
3) At the junction of the internal and external carotid arteries are a cause of thrombotic brain infarcts and can also be a site of origin of emboli.
What are the sites of arrest of arterial emboli?
1) Branches of the carotid artery, most frequently the middle cerebral artery, leading to cerebral infarction.
2) Branches of the mesenteric artery, leading to hemorrhagic infarction of the intestine.
3) Branches of the renal artery, producing characteristic wedge-shaped pale infarcts of the renal cortex.
What is a paradoxical emboli?
Left-sided emboli that originate in the venous circulation but gain access to the arterial circulation through a right-to left-shunt, most often a patent foramen ovale or an atrial septal defect.
What is a fat emboli?
1) Particles of bone marrow and other fatty intraosseous tissue that enter the circulation as a result of severe fractures.
2) Lodge in the lungs, brain, kidneys, and other organs.
3) May be asymptomatic or may be manifest clinically by the potentially fatal fat embolism syndrome, characterized by pulmonary distress, cutaneous petechiae, and various neurologic manifestations.
What is an air emboli?
1) Results form the introduction of air into the circulation, most often by a penetrating chest injury or as a consequence of a clumsily performed criminal abortion.
2) Can occur as decompression sickness, observed in deep-sea divers who return to the surface too rapidly. Bubbles of relatively insoluble nitrogen come out of solution and obstruct the circulation, producing musculoskeletal pain and small infarcts in the central nervous system, bones, and other tissues. Because nitrogen has an affinity for adipose tissue, obese persons are at increased risk for this disorder.
What is an amniotic fluid emboli?
1) Are caused by escape of amniotic fluid into the maternal circulation.
2) Can activate the coagulation process, leading to DIC.
3) Can cause maternal death.
Name three miscellaneous sources of emboli.
1) Fragments of atherosclerotic plaques
2) Clumps of inflamed infected tissue
3) Tumor fragments
List five causes of edema.
1) Increased hydrostatic pressure
2) Increased capillary permeability
3) Decreased oncotic pressure
4) Increased sodium retention
5) Blockage of lymphatics
List six types of edema.
1) Anasarca; generalized edema
2) Hydrothorax; accumulation of fluid in pleural cavity.
3) Hydropericardium; abnormal accumulation of fluid in the pericardial cavity.
4) Hydroperitoneum (ascites); abnormal accumulation of fluid in the peritoneal cavity
5) Transudate
6) Exudate
Define transudate.
1) Noninflammatory edema fluid that results from altered intravascular hydrostatic or osmotic pressure.
2) Has a low protein content and a specific gravity less than 1.012
Define exudate.
1) From increased vascular permeability as a result of inflammation.
2) High protein content, a specific gravity exceeding 1.020 and characteristically contains large numbers of inflammatory leukocytes.
3) Because the metabolically active leukocytes consume glucose, the glucose content is often greatly reduced.
Describe edema caused by increased hydrostatic pressure.
1) Exemplified by CHF.
2) Right-sided failure results in peripheral edema.
3) Left-sided failure results in pulmonary edema.
Describe edema caused by increased capillary permeability.
Occurs in inflammation or with injury to capillary endothelium, as may occur in burn injury.
Describe edema caused by decreased oncotic pressure.
1) It's from hypoalbuminemia caused from: protein loss in the kidney (nephrotic syndrome), decreased production of albumin in cirrhosis of the liver.
Describe edema caused by increased sodium retention.
1) Can occur as either a primary or secondary phenomenon
2) Primary sodium retention, associated with renal disorders
3) Secondary sodium retention, such as occurs in CHF
What is secondary sodium retention that occurs in CHF?
1) Decreased cardiac output in decreased renal blood flow, which activates the renin-angiotensin system.
2) In turn, this activates aldosterone production, with resultant retention of sodium and water.
What is shock?
Circulatory collapse with resultant hypoperfusion and decreased oxygenation of tissues.
What are the causes of shock?
1) Decreased cardiac output, as occurs in hemorrhage or severe left ventricular failure.
2) Widespread peripheral vasodilation, as occurs in sepsis or severe trauma, with hypotension often being a prominent feature.
What are four types of shock?
1) Hypovolemic
2) Cardiogenic
3) Septic
4) Neurogenic
What is hypovolemic shock?
1) Circulatory collapse resulting from the acute reduction in circulating blood volume caused by:
2) Severe hemorrhage or massive loss of fluid form the skin, from extensive burns, or from severe trauma.
3) Loss of fluid from the gastrointestinal tract, through severe vomiting or diarrhea.
What is cardiogenic shock?
Circulatory collapse resulting from pump failure of the left ventricle, most often caused by massive myocardial infarction.
What is septic shock?
1) Characteristically associated with G- infections causing endotoxemia; also occurs with G+ and other infections.
What happens in septic shock?
1) Initially, vasodilation may result in an overall increase in blood flow. however, significant peripheral pooling of blood from peripheral vasodilation results in relative hypovolemia and impaired perfusion.
2) Lipopolysaccharide adn other bacterial products appear to induce a cascade of cytokines, activate complement components and the kinin system, and cause direct toxic injury to vessels.
3) Endothelial injury can lead to activation of the coagulation pathways and to DIC.
4) Another toxic molecules, the so-called superantigens, produces septic shock-like manifestations. The release of these molecules occurs in teh "toxic shock syndrome", which is most often associated with S. aureus infection.
What is neurogenic shock?
Most often associated with severe trauma and reactive peripheral vasodilation.
What is the nonprogressive (early) stage of shock?
Compensatory mechanisms, including increased heart rate and increased peripheral resistance, maintain perfusion of vital organs.
What is the progressive stage of shock?
Characterized by tissue hypoperfusion and the onset of circulatory and metabolic imbalance, including metabolic acidosis from lactic acidemia. compensatory mechanisms are no longer adequate.
What is the irreversible stage of shock?
Organ damage and metabolic disturbances are so severe that survival is not possible.
What are the morphologic manifestations of shock?
1) Wide variety of anatomic findings are observed in shock The most important of these is acute tubular necrosis of the kidney, which is potentially reversible with appropriate medical management.
2) Areas of necrosis in the brain
3) Centrilobular necrosis of the liver
4) Fatty change in the heart or liver
5) Patchy mucosal hemorrhages in the colon.
6) Depletion of lipid in the adrenal cortex.
7) Pulmonary edema