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54 Cards in this Set
- Front
- Back
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What factors are involved in the intrinsic pathway
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Factor XII (Hagelman Factor)
Factor XI Factor IX Factor VII |
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What factor in the intrinsic pathway is activated by another factor in the extrinsic?
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Factor VII in extrinsic activates factor IX in intrinsic
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Describe the common pathway
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X---->Xa (via Factor VIII or VII)
Prothrombin----->Thrombin Fibrinogen----->Fibrin |
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Factor #: Thrombin
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IIa
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Factor # Fibrin Stabilizing Factor
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XIII
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Fibrin Stabilizing Factors is what number?
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XIII
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What are the two regulators of Plasminogen Activator and where do they act?
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Plasminogen Activator Inhibitor = sheath around Plasminogen
Alpha-2 Antiplasmin inactivates free Plasmin |
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Where do we find white and red infarcts?
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Red Infarcts = Venous occlusions in organs with single outflow (testies, ovaries), loose tissue that allows blood to collect, dual circulation tissues (lung, small intestines), when flow is reestablished
White = arterial occulsion, and solid tissues where hemorrhage is limited (heart, spleen, kidney) |
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stimuli for acute inflammation
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microorganism infection
physical agents (burns, radiation) chemical agents necrotic tissue foreign bodies immunologic reactions |
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mediators fo vasodilation:
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histamine
prostoglandin nitric oxide |
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Transudate vs Exudate
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Exudate is fluid with high protein content that occurs during inflammatory response because the reiteration of endothelial cells.
Transudate is edema with low protein content from a decrease in colloid osmotic pressure and an increase of hydrostatic pressure. |
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Chemical mediators of vascular permeability
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Histamine
Bradykinin C3a, C5a Leukotrienes PAF |
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Receptors involved in Loose Adhesion
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Selectins on Endothelial Cells
Siayl-Lewis X receptor on leukocytes |
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Receptors involved in firm adhesion
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Integrins on Leukocytes
ICAM-1, VCAM 1 on endothelial cells |
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Receptors and enzymes involved in diapedesis
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PECAM-1 on leukocytes and endothelial cells
proteases to break through junctions |
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chemotactic factors
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C5a
Leukotriene B4 Chemokines Bacterial products |
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With pseudomonas what cell predominates?
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Neutrophils. No lymphocyte action
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Two PAMPS we need to know
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Formyl Peptides
Unmethylated CpG DNA motifs |
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Oxygen dependent killing mechanisms. Where is each found?
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Formation OH- via NADPH oxidase (found in neutrophils and macrophages). OCL is found only in neutrophils which have MPO
Using Arginine to make OONO via iNOS , |
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Oxygen-INdependent killing mechanisms
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lysozyme, lactoferrin, bacterial permeability protein, major basic protein, defensins
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What defect hurts firm adhesion?
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Leukocyte Adhesion Deficiency I = Defective Leukocyte Integrins
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Defective Leukocyte Integrins = ?
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Cant firm adhere, Leukocyte Adhesion Deficiency I
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Defective Loose Adhesion is consequence of what?
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Lack of Sialyl-Lewis X on Leukocytes. Called Leukocyte Adhesion Deficiency II
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What disease causes a defect in NADPH oxidads? Whats the consequence?
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Chronic Granulamatous Disease, Formation of Granulomas.
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What goes wrong in Chediak-Higashi Sydrome?
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Vesicle transport problem. Lyzosomes don't fuse with phagosomes and you have defective phagocytosis. Find chunky granules in neutrophils and ocular and skin hypo pigmentation.
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what factors are involved in termination of acute inflammation?
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Lipoxines (Arachadonic Acid pathway)
Anti-inflammatory cytokines by macrophages, other cells (IL-10, TGF-Beta) |
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Roles of Kinins?
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Vasodilation
Pain Amplification |
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Roles of C3a, C5a
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Vasodilation, chemotatic vasopermeability
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When fibrin is broken down, what is formed and what does it do
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its broken down into fibrin degradation products, which increase vascular permeability
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What prostaglandin causes fever and pain?
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PGE 2
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Classical Pathway
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- Adaptive
- IgM and IgG bind to antigens and complements bind to FC region. -C1a, C1r and then C1s form together, cleave C4, Cleave C2 -formation of C3 convertase, cleaves C3 -formation of C5 convertase, cleaves C5 - C5 associates with C6,C7, C8---> PORE |
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Lectin Pathway
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Mannose binding LEctin in liver binds to Mannans and MASP 1 and MASP 2 = complex which cleaves C4 and C2 to form C3 convertase
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Alternative Pathway
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Antibody Independent.
Spontaneous C3 breakdown into C3a, C3b by Kallikrein, Plasmin, or Elastase. This is controlled by Salic Acid C3b attaches to the cell surface interacts with factor B and D, to become C3 convertase with factor P to stabilize it. |
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Why don't we attack our own cells? What prevents compliment?
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Decay Accelerating Factor": accelerates C3 convertase in blood
CD59: Cell surface protein that kicks almost finished MACs off before punching holes (it keeps C9 from binding) |
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What is the role of Salic Acid?
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Salic Acid on cells in Mammels prevents attachment of C3b
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Paraxysmal Nocturnal Hemoglobinuria
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Lack of protection from N
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Key mediators of increased vascular permeability
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histamine, bradykinin, C3a and C5a, leukotrienes, PAF
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mediators of vasodilation
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histamine, prostaglandins, nitric oxide initially
IL-2 and TNF later |
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Examples of chemotactic cytokine
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Attract immune cells; Example:
IL-8 (neutrophils) RANTES: monocytes, T cells MCP-1, MIP-1 |
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Nitric Oxide
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Acts as a local mediator to cause vascular smooth muscle relaxation and vasodilation, reduce leukocyte adhesion and platelet adhesion.
Also synthesized by macrophages for killing bacteria. |
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Most important chemotactic factors in acute inflammation
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C5a, leukotriene B4, Chemokines (IL-8, MCP-1), Bacterial Products (N-formyl-methionyl peptides)
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3 ways you can get fatty liver with ethanol toxicity?
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- increased expression of genes leading to increased synthesis of triglycerides (SREBPs)
- impairs microtubular function and have decreased secretion of lipoproteins resulting in intracellular fat accumulation - NAD depletion and this is needed for breakdown of FFA = FFA accumulation |
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Platelet Aggregation and Adhesion
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GpIb receptor + von Willibrand factor ----> platelet changes shape and there is release reaction (you need normal platelet prostaglandin synthesis).
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Most important chemotactic factors in acute inflammation
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C5a, leukotriene B4, Chemokines (IL-8, MCP-1), Bacterial Products (N-formyl-methionyl peptides)
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3 ways you can get fatty liver with ethanol toxicity?
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- increased expression of genes leading to increased synthesis of triglycerides (SREBPs)
- impairs microtubular function and have decreased secretion of lipoproteins resulting in intracellular fat accumulation - NAD depletion and this is needed for breakdown of FFA = FFA accumulation |
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Platelet Aggregation and Adhesion
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GpIb receptor + von Willibrand factor ----> platelet changes shape and there is release reaction (you need normal platelet prostaglandin synthesis).
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How is Bradykinin made? What is its role?
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XIIa cleaves prekallikrein to Kallikrein.
Kallikrein cleaves HMWK to Kinins. Role = vasoactive mediator, pain, amplification for actue inflammation! |
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Ray's Disease
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Mitochondrial injury (salicylates) ---> ATP depletion, decreased fatty acid oxidation --> Microvesicular fatty change ---> Reye Syndrome!
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Acetaminophen Toxicity
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glucoronide or sulfate.....
If lots ---> CYP2E1 creates a reactive intermediate which is neutralized by GSH.... |
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Why are children more susceptible to acetaminophen toxicity?
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Because they don't have glucuronide.
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What do you treat people with for acetaminophen toxicity?
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N-acetylcysteine ---> Cysteine
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chronic effects of ethanol
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1) direct toxicity of ethanol and its metabolites: acetylaldehyde can induce lipid peroxidation and form protein adducts
2) Free radicals are generated by by-products during metabolism |
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Lesions involved in creation of alcoholic cirrhosis
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Earliest lesions around the central vein; then perisinusodial fibrosis, due to conversion of stellate cells into fibroblasts in the space of Disse. Collagen synthesis and degradation by mediators of peptide growth factors.
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Ischemia: What is seen early that is usually seen late
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Calcium influx and plasma membrane damage associated with it.
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