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210 Cards in this Set
- Front
- Back
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3 cellular responses to stress?
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1. Adaptation
2. Cell injury 3. Cell death (Irreversible injury) |
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What is the most important cause of hypoxia?
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Ischemia
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Cell injury is most likely to affect which cellular components?
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1. Cell membranes (almost always)
2. Mitochondria (compromise ATP production) |
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What are the 4 cellular ADAPTIVE changees to stress?
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1. Hypertrophy
2. Hyperplasia 3. Atrophy 4. Metaplasia |
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What adaptive change occurs when there is increased functional demand on cell & specific hormonal stimulation?
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Hypertrophy
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Physiologic hyperplasia can be caused by? (2)
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1. Hormones
2. Compensatory |
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Pathologic hyperplasia is usually due to?
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Excessive hormonal or growth factor stimulation
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What proteolytic systems are involved in atrophy? (2)
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1. Ubiquitin-proteasome pathway
2. Autophagy |
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Reversible change in which one adult cell type is replatced by another adult cell type is known as?
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Metaplasia
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What are the 2 types of reversible injuries?
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1. Cellular swelling
2. Fatty change |
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What is the most common type of reversible cell injury?
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Cellular swelling
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What causes cellular swelling to occur?
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Incapable of maintaining ionic & fluid homeostatis
-Increased membrane permeability or damaged Na pump -Membrane damage or loss of ATP |
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Fatty change is most frequently seen in which cell type?
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Hepatocytes
Cells involved in fat metabolism OVerproduction of fat |
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Morphologic appearance of necrosis is result of which 2 processes?
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1. Enzymatic digestion
2. Denaturation of proteins |
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What are the 2 processes of enzymatic digestion of the cell?
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1. Autolysis- hydrolytic enzymes from dead cells themselves
2. Heterolysis-enzymes derived from lysosomes of leukocytes |
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What are the 3 microscopic hallmarks of necrosis?
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1. Karyolysis
2. Pyknosis 3. Karyorrhexis |
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Which microscopic hallmark of necrosis features fading of the nucleus?
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Karyolysis
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Which microscopic hallmark of necrosis features shrinkage & darkening of nucleus due to dentaturation of nuclear proteins?
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Pyknosis
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Which microscopic hallmark of necrosis features fragmentation of pyknotic or partially pyknotic nucleus?
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Karyorrhexis
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What are the 6 patterns of tissue necrosis?
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1. Coagulative necrosis
2. Liquefactive necrosis 3. Gangrenous necrosis 4. Caseous necrosis 5. Fat necrosis 6. Fibrinoid necrosis |
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What are most predominant types of tissue necrosis?
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Coagulative necrosis
Liquefactive necrosis |
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What type of necrosis is characterized by denturation of proteins and is characteristic of hypoxic death of all tissues except brain?
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Coagulative necrosis
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What type of necrosis is classically seen in MI?
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Coagulative necrosis
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What type of necrosis is characteristic of focal bacterial infections & hypoxic death of CNS due to catalytic degreadation of cell structures?
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Liquefactive necrosis
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What type of necrosis is seen due to compromised blood supply of a limb, often secondarily to bacterial infection?
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Gangrenous necrosis
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In dry gangrene what type of necrosis predominates?
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Coagulative necrosis
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In wet gangrene what type of necrosis predominates?
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Liquefactive necrosis
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TYpe of coagulative necrosis encountered in TB-- dry, white, cheesy appearance
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Caseous necrosis
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What term applies to focal areas of fat destructiion resulting from abnormal release of activated pancreatic enzymes into pancreas or peritoneal cavity/
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Fat necrosis
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What type of necrosis usually occurs w/ immune-mediated reactions involving blood vessels-- Ab-Ag complexes combine to w/ fibrin to form pink amorphous layer?
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Fibrinoid necrosis
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What is the major mechanism of apoptosis?
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Activation of caspase family of enzymes which breakdown nuclear & extranuclear cell proteins
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What are examples of subcellular responses to injury? (4)
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1. Autophagy
2. Induction of SER 3. Mitochondria alterations 4. Cytoskeletal abnormalities |
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What cellular response produces an undigested residual pigment called lipofuscin pigment after intracellular lipid peroxidation?
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Autophagy
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What are the exogenous pigments? (4)
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1. Anthracosis
2. Silicosis 3. Siderosis 4. Tattoo |
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What are the endogenous pigments? (4)
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1. Lipofuscin
2. Melanin 3. Hemosiderin 4. Bilirubin |
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Which pigment is due to carbon dust particles accumulating in macrophages of lung but doesn't usually cause probelms?
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Anthracosis
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Which type of pigment causes significant lung disease due to contamination w/ silicone particles?
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Silicosis
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Which type or pigment usually doesn't cause problems but is a contaminatior of Fe particles?
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Siderosis
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Golden yellow to brown pigment derived from hemoglobin breakdown & is a form of stored iron?
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Hemosiderin
Hemosiderosis-- systemic overload of iron |
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Disease of extreme iron overload?
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Hemochromatosis
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Brown green pigment derived from hemoglobin normally seen in bile?
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Bilirubin
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When necrotic debris is not rapidly removed by scavenger cells, Ca & other minerals are depositied however, Ca levels & metabolism are normal
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Dystrophic calcification
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What is it called when deposition of Ca salts in vital tissure due to increased levels of Ca (hypercalcemia)?
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Metastatic calcification
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Most common trigger of acute inflammation?
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Infection
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What is the first vascular change to occur in acute inflammation?
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Vasodilation
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Once vasodilation occurs in acute inflammation, what occurs next?
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Hyperemia (Increased blood flow) --> Increased permeability
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Increased permeability of microvasculature in acute inflammation causes?
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Exudation of protein-rich blood fluid into extravascular tissue
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What is the HALLMARK of early hemodynamic changes in acute inflammation?
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Hyperemia
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When exudation occurs during acute inflammation what occurs next?
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STASIS
Concentration of RBC --> Increased blood viscosity --> Slowing of circulation |
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Once stasis occurs, the next step in acute inflammation is?
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Margination of leukocytes & emigration of leukocytes to cause extravascular events
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What are the sequence of events that lead to exudation? (5)
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1. Vasodilation & hyperemia
2. Increased hydrostatic pressure 3. Increased filtration of fluid from capillaries (Transudation) 4. INcreased permeability 5. Escape of protein rich plasam (Exudation) |
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What are the sequence of events that follow exudation? (3)
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1. Decreased intravascular osmotic pressure
2. Increased osmotic pressure of interestital tissue 3. Marked outflow of plasma fluid & its accumulation into interstitial tissue (EDEMA) |
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What is the sequence of cellular events that occur during acute inflammation? (4)
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1. Margination & rolling
2. Adhesion & transmigration 3. Chemotaxis & activation of leukocytes 4. Phagocytosis |
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Loose adhesion & selections are involved in what cellular event of acute inflammation?
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Margination & rolling
-WBC move toward periphery of vessel & roll along endothelium |
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Firm adhesion & integrins are involved in what cellular event of acute inflammation?
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Adhesion & Transmigration
-Endothelial cell adhesion of immunoglobulins (ICAM & VCAM) to integrins on leukocytes |
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What is the main mediator of diapedesis in transmigration of leukocytes in acute inflammation?
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PECAM-1
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What are the main chemotactic factors involved in acute inflammation?
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1. Bacterial products
2. Il-8 (cytokines) 3. C5a (complement) 4. LTB4 (products of AA metabolism) |
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Which cells predominate during the first 6-24 hrs of acute inflammation?
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Neutrophils
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Which cells predominate during subsequent 24-48 hrs in acute inflammation?
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Monocytes
-May persist for long periods as tissue macrophages |
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What are the 3 steps of phagocytosis?
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1. Recognition & attachment of partical to be ingested
2. Engulfment 3. Killing & degradation |
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Recognition & attachment of phagocytes is accomplished when particle is coated by?
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Opsonins
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Which substances act as opsonins in acute inflammation? (3)
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1. C3b
2. IgG 3. Collectins |
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What are the cardinal signs of acute inflammation? (5)
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1. Heat (calor)
2. Redness (rubor) 3. Swelling (tumor) 4. Pain (dolor) 5. Loss of function (functio laesa) |
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What is the earliest mediator of acute inflammation?
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Histamine
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What are the actions of histamine? (3)
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1. Vasodilation
2. Increased vascular permeability of venules 3. Chemotactic for eospinophils |
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What causes activation of Hageman factor (Factor XII)? (3)
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1. Collagen
2. Basement membrane 3. Activated platelets |
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What chemical mediatior is released from stimulated platelets during aggregation & has similar effects to histamine?
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Serotonin
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What are the 4 plasma protease systems initiated by Hageman factor (Factor XII)?
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1. Kinin system
2. Clotting system 3. Fibrinolytic system 4. Complement system |
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Activation of kinin system leads to formation of?
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Bradykinin
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Bradykinin is derived from?
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Plasma precurosr high-molecular weight kininogen (HMWK)
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What cleaves HMWK to form bradykinin?
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Kallikrein
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What are the actions of bradykinin? (3)
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1. Vasodilation
2. Increased permeability of venules 3. Pain |
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What phase of inflammation is bradykinin?
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Early phase
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What are the actions of Factor Xa as a chemical mediator of inflammation? (2)
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1. Increased vascular permeability
2. Mediates leukocyte transmigration |
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What are the actions of Thrombin as a mediator of inflammation? (2)
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1. INcreased leukocyte adhesion
2. Generates fibrinopeptides |
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What are the actions of fibrinopeptides as mediators of inflammation? (2)
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1. INcreased vascular permeability
2. Chemotactic for leukocytes |
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What are the actions of plasmin as a mediator of inflammation? (3)
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1. Activates Hageman factor
2. Cleaves C3 -> C3a (increase vascular permeability) 3. Degrades fibrin to form fibrin-degredation produces (increased permeability) |
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What is the critical step of complement cascade?
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Activation (cleavage) of C3
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Which complement pathway is most important in acute inflammation?
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Alternate pathway
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What are the actions of C3a as a mediator of inflammation? (2)
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1. Increased vascular permeability --> stimulates histamine release
2. Anaphylatoxin (role in immediate hypersensitivity reactions) |
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What are the actions of C5a as a mediator of inflammation? (
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1. Increased vascular permeability (anaphylatoxin)
2. Increases adhesion 3. Chemotactic 4. Activates lipooxygenase pathway of AA metbolism |
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Which prostaglandins cause vasodilation? (4)
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1. PGI2
2. PGE2 3. PGE1 4. PGD2 |
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Which prostaglandin causes pain & fever?
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PGE2
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Which prostglandins cause increased vascular permeability? (2)
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1. PGD2
2. PGE2 |
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Which leukotrienese cause increased vascular permeability? (3)
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1. LTC4
2. LTD4 3. LTE4 |
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Which leukotriene causes chemotaxis & leukocyte adhesion?
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LTB4
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What are the most important mediators in late, sustained phase of acute inflammation?
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Prostaglandins & leukotrienes
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Which leukotriene does NOT cause increased vascular permeability?
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LTB4
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Which cytokines act as mediators of acute inflammation? (4)
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1. Interleukin-1
2. Tumor necrosis factor TNF 3. Interferon-gamma 4. Chemokines (Il-8) |
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What are the actions of Il-1 & TNF? (4)
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1. Fever (systemic acute phase reactions)
2. Leukocyte adhesion 3. Stimulation of other mediators 4. Aggregation & activation of neutrophils (TNF) |
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What are the actions of INF-gamma? (3)
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1. Activator of macrophages & neutrophils
2. Upregulate enzymes that produce oxidative burst 3. Stimulate synthesis of NO synthase |
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What are the actions of Il-8 as a mediator of inflammation? (2)
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1. Powerful chemoattractant
2. Activator of neutrophils |
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What are the effects of NO during inflammation? (3)
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1. Vasodilation
2. Antagonist to adhesion effects 3. Microcidal agent |
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What are the defining characteristics of chronic inflammation? (3)
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1. Infiltration of mononuclear leukocytes (lymphocytes, plasma cells, macrophages)
2. Tissue destruction 3. Angiogenesis & fibrosis |
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What is a major stimulator of monocytes & macrophages?
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Interferon-gamma (lymphokine)
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What type of inflammation is characterized by exudation of thin, watery (serous) fluid?
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Serous inflammation
ex: skin blister from sunburn |
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What type of inflammation is seen in acute inflammation & is characterized by fibrinous exudation?
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Fibrinous inflammation
ex: acute rheumatic carditis |
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What type of inflammation is seen in acute inflammation & is characterized by production of large amounts of pus or purelent exudate?
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Suppurative (purulent) inflammation
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Abscesses are localized collections of pus often caused by ?
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Staphylococci
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Cellulitis is a spreading edematous & purulent inflammation often caused by?
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Streptococci
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Surface has no epithelium but is instead covered by fibropurulent exudate & has superfiical zone of acute inflammation & may have deeper zone of chronic inflammation & scarring?
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Ulcer
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Pattern of chronic inflammation which is characterized by presence of granulomas?
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Granulomatous inflammation
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Granulomas consist of?
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1. "Epitheloid appearnce of macrophages
2. Lymphocytes 3. Plasma cells 4. Multinucleated giant cells |
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What are the 2 ways in which repair can be accomplished?
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1. Regeneration by parenchyma
2. Replaced by CT = fibrosis |
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Cells that continue to multiply throughout life to replace shed or destroyed cells.
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Labile tissues
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Which types of tissues are LABILE? (3)
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1. Epithelium (skin, mucosa, GI, urinary)
2. Some ductal epithelium of exocrine glands 3. Stem cells in BM & lymphoid organs |
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Cells that retain latent capacity to regenerate but do not normally actively replicate.
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Stable (Quiescent) Tissues
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Which types of tissues are STABLE (QUIESCENT)? (2)
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1. Parenchyma of most solid glandular organs (liver, pancreas, kidney, parotid..)
2. Mesenchymal cells (fibroblasts, endothelial cells, smooth muscle) |
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Terminally differentiated cells that have essentially no regenerative capacity once growth is complete
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Permanent (Non-dividing) Tissues
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What types of tissues are permanent (non-dividing)? (3)
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1. Most neurons
2. Cardiac muscle cells 3. Skeletal muscle cells |
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Growth factors which induce expression of genes that control normal cell growth pathways?
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Proto-oncogenes
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Alterations of proto-oncogenes that may contribute to uncontrolled cell growth like cancers
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Oncogenes
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Which growth factor stimulates keratinocyte migration & granulation tissue formation?
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Epidermal growth factor (EGF)
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Which growth factor stimulates proliferation & motility of endothelial cells in angiogenisis?
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Vascular endothelial growth factor (VEGF)
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Which growth factors recruit & stimulate fibroblasts? (3)
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1. PDGF
2. FGF 3. TGF-beta |
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Collagen synthesis is induced by which growth factors? (5)
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1. TGF-beta
2. PDGF 3. FGF 4. Il-1 5. TNF |
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Net collagen accumulation in scar formation is due to?
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Increased collagen synthesis & reduced collagen degredation
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Which degrades collagen & ECM components?
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Matrix metalloproteinases (MMPs) which are Zn dependent
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When does healing by first intention occur?
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When clean uninfected surgical wound margins can be closely approximated w/ sutures
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What occurs during the first 24 hrs of healing by 1st intention? (2)
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1. Fibrin clot --> scab
2. Acute inflammation- neutrophils |
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What happens within 24-48 hrs of healing by 1st intention?
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Epithelial cells bridge wound
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What happens by day 3 of healing by 1st intention? (2)
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1. Neutrophils replaced by macrophages
2. Granulation tissue begins growing |
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What happens by day 5 of healing by 1st intention? (2)
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1. Granulation tissue fills space completing bridge
2. Epithelium reaches full thickness |
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What happens during the second week of healing by 1st intention?
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Blanching begins
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When does healing by 2nd intention occur?
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Large tissue defect & primary closure wound margins cannot be attained
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In healing by 2nd intention what cells are involved in debriding the wound?
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Macrophages
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When does surface reepithelialization occur during healing by 2nd intention?
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surface reepithelialization occurs AFTER granulation tissue has bridged
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In healing by 2nd intention, granulation tissue will only grow into an area of wound if?
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It has been debrided by macrophages
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Which step of healing by 2nd intention is unique?
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Wound contraction occurs to decrease gap
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What are the main differences of healing by 1st intention & 2nd?
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1. 2nd intention takes longer & timing is less predictable
2. 2nd- inflammation is more intense & prolonged 3. Wound contraction occurs within 6 weeks- myofibroblasts |
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What is the most important cause of delayed wound healing?
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Infection
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What causes keloid formation?
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Excessive amounts of collagen give rist to protruding scare -- due to inadequate rate of lysis of fibrous proteins
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What are the 3 major factors in pathogenesis of edema?
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1. Increased hydrostatic pressure
2. Reduced plasma osmotic pressure 3. Lymphatic obstruction |
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What are the 2 ways in which increased hydrostatic pressure can be caused?
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1. Impaired venous return
2. Arteriolar dilation |
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Right sided CHF manifests with edema of?
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Right sided CHF
-Generalized edema of skin & subcutaneous tissues -- especially persistent swelling of feet & ankles |
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Left sided CHF manifests w/ edema of?
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Left sided CHF
-Pulmonary edema |
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In which 2 ways can reduced osmotic pressure of plasma cause edema?
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1. Excessive loss of albumin
2. Decreased synthesis of albumin |
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Very severe generalized edema of skin & subcutaneous tissues?
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Anasarca
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Transudate in chest cavities
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Hydrothorax
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Edema in pericardial sac
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Hydropericardium
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Transudate in abdominal cavity
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Asictes (hydroperitoneum)
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Lymph in tissues due to removal of lymph nodes
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Lymphedema
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Significant edema that causes pit when putting finger pressure
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Pitting edema
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What is hypostatic pneumonia?
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Pulmonary edema can cause fluid in alveolar sacs to trap bacteria
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Hyperemia is process where there is localized increase in blood volume due to?
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Increased inflowing arterial blood
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Congestion is process where localized increased in blood volume is due to?
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Diminished or restricted venous outflow
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What is one of the most reliable postmortem indicators of left ventricular cardiac failure?
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Chronic passive congestion of lungs
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Which 2 conditions are similar in that they both are characterized by local increase in blood volume relation to dilation of small vessels?
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Hyperemia
Congestion |
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What are heart-failure cells?
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Alveolar macrophages filled w/ hemosiderin due to pulmonary edema from left sided CHF
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Nutmeg liver is seen in?
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Right sided CHF causes necrosis around central veins due to increased pressure
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Extravasation of whole blood due to rupture of vessel is known as?
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Hemorrhage
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Ruptured artery that causes a "bruise w/ a bump"
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Hematoma
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Flat bruise usually due to rupture of vein?
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Ecchymosis
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Pinpoint hemorrhages of capillaries?
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Petechiae
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Large flat bruises due to a bleeding problem that do not occur in healthy people
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Purpura
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Hemorrhage ino the chest cavity?
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Hemothorax
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Hemorrhage into pericardial sac?
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Hemopericardium
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Hemorrhage into abdominal cavity?
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Hemoperitoneum
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Hemorrhage into joint space usually due to a serious bleeding disorder
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Hemoarthrosis
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What causes shock?
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Sudden loss of >20% of blood volume
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Formation of blood clot within a non-interrupted vessel of a living person?
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Thrombosis
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What inhibits blood clotting?
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Intact endothelial cells inhibit blood clotting by inhibiting hemostasis & thrombosis
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What are the antiplatelet functions of intact endothelium? (3)
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1. Insulation (barrier)
2. Release PGI2 & NO (prevent sticking) 3. Degredation of ADP (powerful aggregating factor) |
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What are the anti-coagulative functions of intact endothelium? (2)
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1. Release of heparin-like substance
2. Release of thrombomodulin |
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How does release of heparin-like substance help in anti-coagulation of intact endothelium?
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Facilitates the actions of antithrombin III (AT III)
-AT inactivates thrombin & other clotting factors -More potent when bound to heparin-like substance |
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How does release of thrombomodulin help in anti-coagulation of intact endothelium?
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Reduces production of fibrin by speeding up activation of Protein C
-Protein C inhibits clotting -Reduces conversion of fibrinogen to fibrin |
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How do injured endothelial cells promote blood clot formation? (3)
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1. Secrete von Willebrand factor
2. Release tissue factor to activate extrinisc pathway 3. Bind Factors IX & X |
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What are the stages of platelet activation? (3)
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1. Adhesion (vWF)
2. Secretion of ADP & serotonin 3. Aggregation- Thrombin, TXA2, and more ATP |
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What are factors that predispose to thrombus formation? (3)
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1. Injury to endothelium
2. Stasis & tubulence promote platelet adherence 3. Hypercoaguability --> trigger clotting cascade |
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What are the types of thrombi? (3)
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1. Mural thrombus
2. Occlusive thrombus 3. Phlebothrombosis |
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Which type of thrombus is stuck to wall of heart or proximal aorta?
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Mural thrombus
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Which type of thrombus completely blocks blood flow in vessels?
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Occlusive thrombus
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Which type of thrombus forms in veins?
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Phlebothrombosis
-Can be occlusive or non-occlusive |
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What is the most common type of phlebothrombosis?
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Deep venous thrombus
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What are the characteristics of a thrombus? (4)
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1. Pale tan
2. Lines of Zahn 3. Friable (crumble easily) 4. Sticks to vessel wall (vWF) |
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What are the characteristics of a post-mortem blood clot? (4)
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1. Chicken fat clot
2. Currant jelly clot (red) 3. Rubbery 4. Does not adhere to vessel wall |
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What are the fates of a thrombus? (4)
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1. Obstruction --> ischemia
2. Break off & form embolus 3. May be removed by fibrinolytic activity 4. May become organized & recanalized |
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Occlusion of some part of the cardiovascular system by impaction of some mass transported to site through blood stream
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Embolism
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What are the types of emboli by composition? (4)
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1. Thromboemboli
2. Fat embolism 3. Air embolism 4. Amniotic fluid embolism |
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What is the most common type of embolus?
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Thromboemboli
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What are the types of venous emboli? (3)
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1. Pulmonary embolism
2. Saddle embolism 3. Paradoxical embolism |
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what type of embolus travels from veins and lodges in lungs?
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Pulmonary embolism
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What type of embolus blocks bifurcation of pulmonary artery and is deadly within minutes?
|
Saddle embolus
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What type of embolus typically forms in legs but then goes to the brain rather than the heart?
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Paradoxical embolus
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Majority of systemic emboli originate where?
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Mural thrombus of left ventricle
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Localized area of ischemic necrosis within an organ- produced by occlusion of arterial or venous systems
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Infarction
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What are the causes of infarction? (4)
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1. Emboli
2. Occlusive thrombosis 3. Advanced sclerosis 4. Torsion |
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What is the most common cause of infarction?
|
Emboli
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What is the most common cause of MI?
|
Occlusive thrombosis
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What is the gross morpholical shape of an infarct?
|
Wedge-shaped
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When are the first changes of infarct seen histologically?
|
After 4-8 hrs
-No histopahologic evidence if pt dies rapidly |
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What are the most common type of infarcts?
|
White infarcts
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White infarcts are almost always due to?
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Arterial occlusion
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White infarcts are common in what type of organs?
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Solid organs w/ one blood supply
(heart, kidneys, spleen) |
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Red infarcts are usually due to?
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hemorrhage
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Why does hemorrhage into infarct occur? (3)
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1. Loose tissues (lungs & liver)
2. Dual blood supply (lungs, sm intestines, liver) 3. Venous occlusion w/ limited outflow (ovaries & testes) |
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What is the most important factor in determining severity of infarction?
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Availability of alternate blood supply
-Dual blood supply- less risk -Collateral blood supply |
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Systemic hyoperfusion due to reduction in cardiac output or in effective circulating blood volume is known as?
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Shock
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What are the end results of shock? (3)
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1. Hypotension
2. Impaired tissue perfusion 3. Cellular hypoxia |
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What are the 4 types of shock?
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1. Hypovolemic shock
2. Cardiogenic shock 3. Septic shock 4. Neurovascular shock |
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What is the most common type of shock?
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Hypovolemic shock
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What causes hypovolemic shock?
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Reduced blood volume --> diminished venous return --> decreases cardiac output
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What type of shock occurs in pts who develop sudden heart pump failure secondary to MI or arrhthymia?
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Cardiogenic shock
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What happens to blood volume in cardiogenic shock?
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Blood volume remains same
-Problem with reduced cardiac output which decreases perfusion |
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What occurs in septic shock?
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Toxins released --> Peripheral vasodilation --> pooling of blood --> reduce venous return --> reduce cardiac output
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In what types of shock does pooling of blood occur?
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1. Septic shock
2. Neurogenic shock |
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Neurogenic shock results from?
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Overactive parasympathetics
-Collapse of vascular tone --> peripheral vasodilation --> pooling of blood --> venous return compromised |
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What is the universal symptom of all types of shock?
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Hypotension
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In which types of shock is ashen, grey pallor & cool, clammy skin seen?
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Hypovolemic & Cardiogenic shock
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In what types of shock is rosy, flushed skin & warm, moist skin?
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Septic & neurogenic shock
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