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243 Cards in this Set
- Front
- Back
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What are the first line of body defenses?
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Physical, biochemical barriers and mechanical barriers
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What are examples of physical barriers?
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Skin, mucosa, respiratory, GI, GU
Surface of skin is in hospitable to most bacteria (acidic) |
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What are examples of mechanical barriers?
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Tears, ciliary action, coughing, urination
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What are the 3 lines of body defenses against infection?
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1. Anatomical
2. Inflammation -Nonspecific (local and systemic) and begins in seconds 3. Immune response -Slower, more specific, long lasting protection |
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What is inflammation?
Where does it occur? What kind of process is it? |
A biochemical and cellular process
Occurs in the vascular tissue Homeostatic process |
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Inflammation response is _______ and dynamic.
Response is _______ (stereotyped). |
Immediate
Nonspecific |
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T/F
Inflammation and infection are synonymous. |
False
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Location of inflammation designated by suffix _____.
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-itis
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What kind of effects does the inflammatory system have?
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Local and systemic
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In what kind of tissue can the inflammatory response only occur in?
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Living
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Inflammatory response is ________.
-Magnitude of response reduced as resolution proceeds. |
Self-limiting
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What is the purpose behind an inflammatory response? Give the 3 phases
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1. Eliminate the pathological insult
2. Remove the damaged tissue 3. Regenerate/repair the damaged tissue |
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What are the general sequence of events in the inflammatory response? (6 steps)
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1. Recognize injury or infection
2. Induce vascular changes 3. Have a leukocytic infiltration of site - exudate 4. Wall off and confine site 5. Stimulate and enhance immune response 6. Promote healing and/or repair of injured site |
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What are the cardinal signs of acute inflammatory responses?
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1. Redness (rubor)
2. Swelling (tumor) 3. Heat (calor) 4. Pain (dolor) 5. Loss of function (functio laesa) |
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What are the 2 categories of inflammation?
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Acute and chronic
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Acute Inflammation- _____ response to injury. Of short duration and _______.
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Immediate
Self-limiting |
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Chronic- Characterized by prolonged duration and _______ events (e.g. not _______).
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Proliferative
Self-limiting |
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What vascular alteration takes place in acute inflammation?
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Dilation of small arterioles - increased blood flow, followed by slowing (stasis) and an increase in permeability
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What 2 chemical mediators alter the vascular events in acute inflammation?
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1. Cell-derived: preformed or synthesized
2. Plasma-derived |
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What is an example of a cell-derived mediator?
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Mast cell
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What is a mast cell and where are they located?
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Cellular bags of granules located in loose connective tissue
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What are the stimuli for mast cells?
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UV light, chemical/physical injury, complement, immune system, etc.
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What are the 2 ways the inflammatory response can be activiated?
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1. Degranulation of stored material
2. Synthesis of mediators in response to stimuli |
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What are 3 performed materials that contribute to mast cells?
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1. Histamine
2. Neutrophil chemotactic factor 3. Eosinophil chemotactic factor (ECF) |
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Histamine causes _______ and increased _______ of post-capillary venules.
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Dilation
Permeability |
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Does histamine contract or relax endothelial cells?
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Contracts
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What are the 3 histamine receptors and their functions?
What do they all increase? |
1. H1: contracts smooth muscle (other than vascular)
2. H2: gastric acid secretion 3. H3: associated with neural tissue, predominately at pre-synaptic sites Influx of Ca into the mast cell |
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How is histamine inhibited?
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An increase in cAMP in the cell
(Epinephrine) |
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What does neutrophil chemotactic factor do?
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Attracts neutrophils for eventual phagocytosis
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What does ECF do?
What is its most important role? |
Attracts eosinophils to site and limits inflammation
Control other mediators |
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What enzymes do eosinophils have?
What do they degrade? |
Aryl sulfatase B - leukotrienes
Histaminase - histamine |
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What are some stimuli that would release arachadonic acid?
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UV light, chemical/physical injury, complement, immune system, etc.
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How does eicosanoid synthesis occur?
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Via Cox-1 or Cox-2 enzymes
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Cox-1 is ________ and primarily cytoplasmic.
Plays a key role in _________ and ________. |
Constitutive
Gastric mucosal protection and renal hemodynamics |
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Which of the Cox enzymes do platelets mainly contain?
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Cox-1
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Cox-2 is primarily nuclear and is ________ in _______, fibroblasts, _______ by various ________ in response to stress.
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Induced
Endothelial cells Macrophages |
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What material is formed mainly through Cox 2?
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PGI2
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What is PGI2?
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Prostacyclins (Autocoids/eicosanoids/prostanoids)
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Where are prostacyclins synthesized?
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Uninjured endothelial walls of blood vessels
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To what do prostacyclins act as an antagonist?
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Thromboxanes
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Prostacyclins do what 3 things?
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1. Relaxes blood vessels (vasodilate)
2. Inhibits platelet aggregation 3. Bronchodilate |
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What are PGD2 and where do they come from?
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Prostaglandins
Mast cells |
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What 2 things do prostaglandins do?
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1. Inhibit platelet aggregation
2. Bronchoconstriction via TP receptors |
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Where do PGE2 come from?
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Macrophages
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What are PGE2's inflammatory functions?
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-Fever
-Bronchial constriction -Vasodilates arterioles, relax VSM -Potentiates action of kinins on pain -Potentiates actions of kinins and histamine on permeability |
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What are the inhibitory effects that prostaglandins have on the inflammatory response?
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-Decrease lysosomal enzyme release
-Decrease histamine release from mast cells -Decrease macrophage activation and the generation and secretion of some cytokines |
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What do thromboxanes cause and promote?
What is their main source? What does it induce? |
-Causes vasoconstriction through TP receptors
-Promotes degranulation and aggegration -Mainly from platelets -Induces smooth muscle contraction |
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What is the net effect of thromboxanes?
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Permit platelet aggregation at inflammatory site while preventing adherenece to normal vascular endothelium
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Where do leukotrienes come from?
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Arachidonic acid via 5-lipoxyganse enzyme (LTA4, LTB4, LTC4, LTD4, LTE4, LTF4)
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What do leukotrienes act like?
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Histamine but longer acting
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Leukotrienes _______ responsiveness of airway to other bronchoconstrictors and stimulates ______ release.
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Enhances
Cytokines |
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Leukotrienes are a _______ agent for some WBCs.
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Chemotactic
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What is PAF?
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Phospholipid released from other proinflammatory cells and vascular
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What does PAF produce?
What does it activate? |
-Hyperactivity and clinical features of the delayed stage of asthma
-Bronchospasm and increase in permeability Platelets (stop bleeding and release serotonin, histamine, thromboxane) |
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What inhibits PAF?
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Glucocoritcoids
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Macrophages mainly produce _____.
Mast cells mainly produce ______. |
PGE2
PGD2 |
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What are cytokines?
What are they produced from? |
Peptide cell regulators
Mainly from lymphocytes, macrophages, endothelial cells, fibroblasts and other WBCs |
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What 2 reactions are cytokines regulators of?
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1. Inflammatory
2. Immune |
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T/F
Cytokine are produced constitutively |
False
They are synthesized de nova |
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Where do cytokines act?
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Locally and on the target cell, they act on specific high affinity receptors
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Name the 6 types of cytokines.
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1. Interleukins
2. Interferon 3. Transforming growth factor 4. Tumor necrosis factor 5. Colony stimulating factors 6. Lymphokines |
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What are interleukins?
What are they produced by and when? |
-Cytokines-monokines
-Biochemical messengers sent from one leukocyte to another -Produced in infection and injury or antigenic challenge |
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Interleukins induce response of _____ cells to antigen.
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Immune
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Interleukin stimulates ___.
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NO
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What inhibits production and activity of interleukin?
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Glucocorticoids and gold compounds
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What is interferon?
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IFN alpha - cachectin; interferon gamma and beta
-Inducible cytokines synthesized in response to viral stimuli |
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What kind of activity does interferon have?
What kind it induce? |
Antiviral
Fever |
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T/F
Interferon does not have effect on infected cell |
True
Protects other neighboring cells from the insult |
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All interferon are _________, but not virus specific.
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Host specific
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What does TGF increase?
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Interleukin production
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What does TGF mediate?
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Proliferation, differentiation, angiogenesis, cell migration and adherence
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TGF stimulates ______ for wound healing, ______ production
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Wound
Collagen |
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What does TNF increase?
Induce? |
Interleukin production and phagocyte activity
Prostacyclin synthesis |
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TNF is important in _______ shock.
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Endotoxic
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What does TNF enhance?
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Angiogenesis
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What are the colony stimulating factors?
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GCSF, GMCSF
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GCSF plays a major role in ______ production and maturation.
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PMN
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What are colony stimulating factors made by?
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Several cell types (endothelial cells, fibroblasts, macrophages, etc.)
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What produces lymphokines?
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T-cells in response to antigenic stimulation
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Cytokines demonstrate interaction of ______ and _____ systems.
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Immune
Inflammatory |
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Immune system can also _____ mast cell degranulation and ______ complement.
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Activate
Activate |
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What 4 stages of inflammation are cytokines associated with?
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1. Initiation
2. Cell recruitment 3. Debris removal 4. Repair |
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Plasma proteins are involved in inflammation when ________ activated gets cascade of events to activate entire system.
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Pro-enzyme
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What 2 pathways activate complement?
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Classical - (antigen/antibody)
Alternate/lecithin pathway (mannose binding protein) |
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Which pathway does not need prior contact with a pathogen for activation?
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Alternate pathway
Innate immunity |
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Complement is a ______ mechanism of self defense.
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Nonspecific
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Once activated, complement virtually participates in every ______ response.
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Inflammatory
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Which component of complement has a central role in all 3 pathways?
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C3
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What is clotting?
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A plasma protein system that forms a fibrinous exudate or meshwork at the inflammation site to trap exudates and microorganisms and foreign bodies
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What is the main clotting substance?
What is the major enzyme? |
Fibrin (end product from cascasde of events)
Thrombin |
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What activates the clotting system?
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Bacteria, tissue destruction, kinins, Hagemen factor
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Clotting is stimulated by both ______ and ______ pathways.
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Extrinsic and intrinsic
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In clotting:
1. Limits spread of ________. 2. Concentrates microorganisms and foreigns bodies to areas of greatest ______ activity. 3. Forms clot to stop bleed and to provide a framework for _______. 4. Chemotactic/enhance ______. |
1. Infection/inflammation
2. Phagocytotic 3. Healing 4. Kinins |
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________ is the dissolution of a clot.
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Fibrinolysis
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What are the 3 steps of fibrinolysis?
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1. Generation of plasmin
2. Breaks down clots 3. Activates complement |
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What is generated in fibrinolysis?
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Plasmin
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What is XIIa?
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Activated Hagemen Factor
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What is the primary kinin?
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Bradykinin - results from kinin cascade
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Bradykinin provides for a _____, hypotension action
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Slow
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What starts the kinin cascade?
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Kallikerin activator
From Hagment factor XII |
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Kinins:
1. Stimulate nerve endings: _____ 2. _______ - actions on endothelial cells 3. ______ complement. 4. Stimulates _____ 5. ______ permeability 6. |
1. Pain
2. Vasodilation 3. Activates 4. PAF 5. Vascular 6. Chemotaxis |
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By what receptors do kinins work?
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B1 and B2 receptors
B1: induced by inflammation B2: main physiological effect |
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What inactivates bradykinin?
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ACE
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What does ACE inactivate?
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Bradykinin
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The immune system _____ and participates in the ______ process.
______ mast cell activation. |
Activates
Inflammatory Stimulates |
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The immune system activates complement when what complex forms?
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Antigen-antibody complex
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What are the 4 systems activated by Hagemen factor?
Where are they stimulated? |
1. Clotting
2. Fibrinolytic 3. Kinin 4. Complement Plasma |
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What does carboxypeptidase inhibit?
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Complement (C5a)
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What 3 enzymes rapidly destroy many components of inflammation?
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1. Carboxypeptidase
2. Histaminase 3. Aryl sulfatase B |
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H1 receptors ________ inflammation.
H2 receptors ________ inflammatory action. |
Promote (degranulation)
Suppress (inhibits degranulation by increasing cAMP) |
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Summary of vascular effects:
1. All ____ effects 2. Microvascular dilation - (____,_____) 3. Enhanced microvascular - permeability (_____) 4. Leukotaxis (exudation) - (_____) 5. Pain - (_____) |
1. Local
2. Rubor, calor 3. Tumor 4. Tumor 5. Dolor |
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In exudation, blood vessels, especially venules, leak fluid and _____.
____ g% compared to ______ g% in transudate. |
Protein
4-5% 0.2-0.5% |
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Exudation is set with slowing of circulation (viscosity) at inflammatory site and _____ permeability of microvasculature.
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Increased
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Escape of coagulation factors can allow for the formation of the clot to:
1. Prevent escape of _____ from area. 2. Supports ______ cells to perform their tasks. |
1. Exudate
2. Inflammatory |
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In the normal state for exudate formation, hydrostatic forces tend to push fluid into the ______ spaces. Balanced by the _____ force exerted by plasma protein.
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Interstitial
Osmotic |
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Exudate formation:
In acute inflammation, get _____ in and around injured area. |
Dilation
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Exudate formation:
Proteins escape with changes in _______. |
Permeability
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T/F
In exudate formation, plasma is lost and blood becomes more viscous. |
True
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What walls off the area in exudate formation?
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Fibrin
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What are the 7 cells associated with acute inflammation?
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1. Neutrophils
2. Eosinophils 3. Lymphocytes 4. Monocytes 5. Basophils 6. Erythrocyte RBC 7. Platelet |
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What perecentage of WBCs are neutrophils?
What produces them? |
50-70%
Hematopoeitic marrow |
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Neutrophils are classified a _______.
Has ________ (rich in hydrolytic enzymes) |
Granulocyte
Lysosomes |
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Phagocytosis requires _____ and presence of _______.
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Energy
Serum |
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What term is described by enhanced binding of an antigen due to actions of complement or antibodies?
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Opsonization
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Neutrophils can secrete and release _______.
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Cytokines (IL)
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What percentage of WBCs are eosinophils?
What kind of inflammations are they main seen in? |
Allergy
Parasitic Chronic inflammatory lesions |
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Eosinophils appear _____ days after PMN.
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2-3
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What kind of agents do eosinophils respond to?
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Chemotaxic
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Eosinophils secrete substances that ______ some actions of basophils/mast cells
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Neutralize
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What are eosinophils armed with as a granulocyte?
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Potent granule constituents which release extra-cellularly and damage multicellular parasites (peroxidase and neurotoxins)
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What percentage of WBCs are lymphocytes?
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25-35%
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Lymphocytes are seen in _____ stages of most acute inflammation.
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Later
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What is the first cell type seen in viral infections?
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Lymphocytes
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T/F
Lymphocytes are seen in chronic inflammation. |
True
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What can lymphocytes produce?
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Other mediators - cytokines (lymphokines)
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What percentage of WBCs are monocytes?
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3-8%
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T/F
Monocytes are a granulocyte. |
False
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Monocytes undergo _____ at inflammatory site.
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Maturation
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When are monocytes seen?
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In the later stages (24-48 hours) of acute inflammation
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What do monocytes become?
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Macrophages
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What does a mononuclear phagocyte do (macrophage - 'big eater')?
|
Destroys microbes and cleans up area for regrowth
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Monocytes are responsive to ________.
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Lymphokines
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Monocytes are important in ______ phase and in the _____ process.
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Demolition
Healing |
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Monocytes are responsible for _____ processing (via release of _______).
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Antigen
Interleukin-1 |
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What cell type do monocytes act as?
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Secretory
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Monocytes respond to ______ agents.
What are these agents? |
Chemotaxic
Kinins, complement, PMNs, bacterial products, etc. |
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What percentage of WBCs are basophils?
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0-1%
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Basophils are _____ than PMN.
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Larger
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Basophils need a _____ signal.
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Chemotaxic
Complement, kinins |
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What role do erythrocyte RBCs have in acute inflammation?
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No real role in combat but can be seen in exudative material
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Platelets are cytoplasmic fragments from ___ _____ in bone marrow.
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Mega karyocytes
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T/F
Platelets have no DNA. |
True
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About how long do platelets live?
|
10 days
|
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When platelets degranulate, what do they release?
|
Serotonin, histamine, PDGF
|
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What do platelets stop?
|
Bleeding and the exudative process
|
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Platelets generate _____ and ______.
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Thromboxane and PAF
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What are the 3 steps of leukocyte infiltration (blood sludging)?
|
1. Margination
2. Pavementation 3. Diapedesis |
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Margination:
Neutralize _______ on cell surface. |
Electronegative charge
|
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Pavementing:
Need what 4 things? Adhesion molecules on leukocytes, _____, and endothelial cells, ______. |
Ca, TNF, LTB, IL
Integrin Selectin |
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Diapedesis:
Stepping across the ______. |
Membrane
|
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What is the purpose of exudate?
|
1. Carrier of therapeutic agents to site
2. Contain endogenous antibacterial agents - complement 3. May contain antibodies 4. Dilute irritating agents/bacterial toxins 5. Fibrin to stop spread of inflammatory area |
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Those who have neutropenia have a shortage of _____ in the blood.
|
Neutrophils
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Where do PMNs come from?
|
Bone marrow
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What are the concentrations that classify the following?
1. Normal WBC 2. Neutropenic 3. Agranulocytosis 4. Leukopenic |
1. 4,000-10,000 cells/microliter
2. <1500-2000 cells/microliter 3. <200 cells/microliter 4. (<4000 cells/microliter of leukocytes) |
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What diseases/treatments can cause neutropenia?
|
Leukemia, drug-induced agranulocytosis, cyclic neutropenia, adrenocorticosteroid
|
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Disorders of Migration and Chemotaxis:
_______ dysfunction - leads to impaired locomotion: _____ ______syndrome. |
Instrinsic cellular
Lazy leukocyte |
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Disorders of migration and chemotaxis:
Extrinsic factors - ex: drugs such as ________. Agents that increase _____ levels in cell may reduce movement of those cells. |
Corticosteroids
cAMP |
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Disorders of migration and chemotaxis:
Deficiencies of chemotactic factors +/- or inactivators of these factors 1. _____ deficiencies (genetic): C3 or C5 2. ________ factor inactivators (CFI): in serum inactivate C3 + C5 (high in those with Hodgkin's disease) |
1. Complement
2. Chemotactic |
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Disorders of phagocytosis are affected in these 3 processes.
|
Attachment, engulfment, destruction
|
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Disorders of phagocytosis:
Defective attachement due to inadequate ________ and in _______ deficiencies. |
Opsonization
Complement |
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What 2 things may be impaired in disorders of phagocytosis?
|
Engulfment and degranulation
|
|
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T/F
Hypogammaglobulinemia can result in a disorder of phagocytosis? |
True
|
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What is an example of a disease whose underlining cause is a disorder of phagocytosis?
|
Chronic granulomatous disease (CGD)
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In CGD, there is a defect in the _____ so that it is incapable of destroying catalase _____ bacteria and fungi since the neutrophil cannot make _______.
|
Neutrophil
Positive H2O2 |
|
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T/F
Catalase negative bacteria are major pathogens in CGD. |
False
|
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T/F
Chronic inflammation can exist without an acute phase. |
True
|
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In chronic inflammation, there is a dense infiltration of _______ and _______ (plasma cells and fibroblasts) compared to neutrophil-rich exudate of acute inflammation.
|
Lymphocytes
Macrophages |
|
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If a macrophage cannot protect its host from tissue damage, the body forms a _______ to wall off and isolate the infected site.
|
Granuloma
|
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Granuloma formation begins when macrophages differentiate into large ________ cells - can survive for weeks.
|
Epithelioid
|
|
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The granuloma itself is walled off or encapsulated by fibrous deposits of ______ and may even be ______.
|
Collage
Calcified |
|
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Classic granuloma is associated with what disease?
|
TB
|
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_______ and _______ are common events at the site of chronic inflammation.
|
Necrosis and fibrosis
|
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Chronic inflammation is a ______ process in which _____ and inflammation are proceeding at the same time as attempts of healing.
|
Prolonged
Destruction |
|
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What are the 5 systemic manifestations in chronic inflammation?
|
1. Hormonal
2. Fever 3. Leukocytosis 4. Elevation in acute phase proteins 5. Increased ESR |
|
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Hormonal systemic manifestations _____ systemic spread of inflammatory response.
Have a feedback loops between inflammatory response and ______ system. |
Inhibit
Neuroendocrine |
|
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Hormonal systemic manifestation:
Pituitary stimulates _______ gland to increase output of _______. |
Adrenal
Glucocorticoids |
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Glucocorticoids exert an _______ effect.
|
Anti-inflammatory
|
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What do glucocorticoids inhibit?
|
Fibroblast proliferation and healing processes
|
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What can glucocorticoids influence?
|
Immune response
|
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What do glucocorticoids reduce?
|
Eosinophils, macrophages, lymphocytes
|
|
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Glucocorticoids ______ protein synthesis.
Large amounts cause _____ of lymph tissue. |
Depress
Atrophy |
|
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This term describes a disturbance of the thermoregulatory function in hypothalamus.
|
Fever
|
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Fever is ______ at higher temperatures.
|
Regulated
|
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What causes fever?
|
Pyrogens, PMNs and monocytes
|
|
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Fever sustains _______ state.
|
Febrile
|
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Arginine vasopressin may be ______ antipyretic.
|
Endogenous
|
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T/F
Fever is protective. |
True
|
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Fever hastens elimination of pathogen and impairs _____ replication. Enhances phagocytosis and production of ______.
|
Viral
Interferon |
|
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T/F
Fever decreases action of antibiotics. |
False
May increase |
|
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What are the stages of fever?
|
1. Cold or chill state
2. Hot or flush state (febrile) 3. Defervescence |
|
|
T/F
Fever is a symptom that should be treated. |
False
Don't want to treat a symptom as may otherwise prolong an infection |
|
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Leukocytosis is an ______ in number of circulating leukocytes.
|
Increase
|
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______ is most commonly overrepresented in leukocytosis.
|
Neutrophil
|
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What are some conditions that increase WBCs?
|
-After strenuous exercise
-Sympathetic reactions -Inflammation and infection (C3 fragment of complement; NRF) |
|
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_____ number of immature neutrophil cells indicate prolonged inflammation.
|
Large
|
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Increased eosinophils may indicate what disorders?
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Allergies, hay fever, parasitic infections (trichinosis), scarlet fever, cholera
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Increased lymphocytes may indicate disorders?
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Whooping cough, infectious mononucleosis, rubella, acute dermatitis
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In viral infections, there is usually an increase in ______ and a decrease in ______.
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Lymphocytes
Neutrophils |
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What proteins are elevated in acute phase inflammation?
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Fibrinogen-clotting, complement, alpha1-antitrypsin, gammaglobulin, C-reactive protein
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CRP is protective and binds to surface of ______ microorganisms. Also may have ______ actions to neutralize proteases, anti-inflammatory cytokines and oxidants.
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Invading
Anti-inflammatory |
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Where are CRPs synthesized?
In response to what? |
Liver
IL-6 |
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CRP may _____ uptake of LDL by macrophages.
Can activate _______. |
Increase
Complement |
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ESR is the only _____ sign.
What is normal for ESR in men? Women? |
Adjunctive
1-13 mm/hr 1-20 mm/hr |
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The healing of local injury calls into play 2 sets of biological processes: _______ and _________ or _________.
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Regeneration
Repair or replacement |
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T/F
All tissues can regenerate. |
False
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______ cells are continuously dividing or a mitotic cell. They constantly replace lost cells.
Typically called _____ cells. |
Labile
Stem |
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______ cells are discontinous replicators or quiescent mitotic cells that normally stop diving when growth ceases.
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Stable
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What are 3 types of regeneration cells?
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1. Labile
2. Stable 3. Permanent cells (non-dividing post mitotic) |
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Repair occurs when ________ is not possible.
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Regeneration
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In repair, replacement of lost tissue by a mass of connective tissue and ultimately a fibrous mass called a _____ (collagen).
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Scar
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The repair process is accomplished by ______ tissue (granulation tissue of healing is highly _________).
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Connective
Vascularized |
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Granulation tissue is rich in what 4 things?
Highly _____ connective tissue. |
1. Macrophages
2. Myofibroblasts 3. Angioblasts 4. Fibroblasts Vascularized |
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There are 2 types of repair: _____ and _________ healing.
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Primary and secondary
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Healing by secondary intention has more repair than _______.
Qualitatively the same but not _______. |
Resolution
Quantitatively |
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Replacement or repair occurs in what 2 overlapping stages?
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Reconstructive and maturation phase
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Reconstructive stage is also know as _____ or fibroblastic phase.
Begins ____ days after initial injury and continues for up to 2 weeks. |
Proliferative
3-4 |
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Reconstructive stage:
Wound is sealed by ______. This provides the meshwork for collagen. |
Fibrin
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Reconstructive stage:
For healing to proceed, fibrin clot must be _______. |
Dissolved
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Reconstructive:
As clot destroyed, _____ tissue formed. Surrounded by _____ and ______. |
Granulation
Macrophages and fibroblasts |
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Reconstructive:
Macrophages secrete _____ for healing. What are these mediators? |
Mediators
Fibroblast activating factor, angiogenesis factor, factors that stimulate epithelial cells to seal wound, secrete collagenases which debrides injured collagen fibers |
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Reconstructive:
Angioblasts appear a few days after incision and serve what 2 functions? |
1. Route for scavenger cells to remove scab and tissue debris
2. Allow influx of blood, oxygen, nutrients |
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What is the term used to describe when the clot/scab is dissolved and granulation tissue is formed so the wound may be protected?
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Epithelialization
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A key cell in the process of reconstruction is the ______.
It is stimulated by the ______. |
Fibroblast
Macrophage |
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What are the cofactors for collagen synthesis?
What happens if these are absent? |
Iron, oxygen, ascorbic acid, alpha-ketoglutarate
Impaired wound healing |
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What forms the scaffold?
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Fibronectin
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What can fibroblasts produce?
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Family of growth factors
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What is the final stage of reconstruction?
This is done via _____ of the granulation tissue. |
Wound contraction
Myofibroblasts |
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The reconstructive phase is characterized by ______ proliferation, epithelialization and _____ differentiation.
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Fibroblast
Cellular |
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When does the maturation phase take place?
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2-3 weeks after injury
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In the maturation phase, _____ tissue is remodeled. Have synthesis of collagen by ______ and lysis by collagenase.
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Scar
Fibroblasts |
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What are the 2 roles of inflammation in clinical medicine?
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1. Rid body of foreign invaders
2. Effectively dispose of damaged material to allow healing to occur |
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If bacteria is not immediately killed, _____ forms.
Irritant allowed to persist - _____ inflammation develops. |
Abscess (pus)
Chronic |
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What are some examples of diseases/injuries in which inflammation does more harm than good?
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Rheumatoid Arthritis
Glomerulonephritis Vasculitis Burn repair |
