Section 1
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5 signs of Acute inflammation
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Date created
Mar 1, 2020
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Section 1
(50 cards)
5 signs of Acute inflammation
Redness Swelling Pain Fever Loss of fuction
Ischemia
Shortage of blood flow, often resulting from obstruction to circulation.
Neutrophils appearance
Segmented nucleus -2-3 lobes. Purple pink granules.
Pyknosis
Nuclear change indicating cell death, condensation of nucleus and clumping of chromatin. Nucleus becomes a dark shrunken mass.
Dendritic Cell function
- Antigen presenting cells - phagocyte and macrophagocytose - Prime T cells.
Hypoxia
Shortage of oxygen, but not complete lack
Lymphocyte function
Mediate immune responses B cells: produce antibody T cells: CD4 T helper cells secretes cytokines (Th1, Th2, 17 and treg) CD8 Cytotoxic cells induce apoptosis in target cell.
Gangrenous necrosis
Form of coagulative necrosis in a limb, appears dark. Ischaemic coagulative necrosis.
Obese with full metabolic dysfunction
INCREASED inflammation, DECREASED metabolic control, DECREASED vascular function.
Metaplasia
reversible change is adult cell type. A change from one cell type to another as a response to chronic injury. e.g. Smoking leads to squamous metaplasia of the bronchi. (ciliated columnar is replaced by squamous).
Embolism
Mobile thrombus, breaks off from thrombus and travels to new location where can cause clot.
Atrophy
DECREASED SIZE OF CELLS, tissues or organs.
Basophils appearance
Large cells with dark large purple granules.
Atrophy can be due to:
Diminished workload Reduced endocrine stimulation Diminished blood supply Loss of innervation Inadequate nutrition
Basophil purpose
Antigen presenting cell to drive Th2 responses. - secrete histamine, leukotrienes. - numbers are increased in allergic reactions. Can bind IgE
Cardiac tamponade
Compression of the heart due to accumulation of fluid in the pericardial sac. leads to rupture of heart wall. Prevents the heart from beating
Eosinophil purpose
Release granules that contain: -major basic protein - eosinophil cationic protein - Peroxidase
Thrombosis
Formulation of a clotted mass of blood (thrombus) in cardio vascular system.
Eosinophil appearance
Large cells with multilobed nucleus and large orange granules.
Autophagy
Intracellular degradation, self digestion. Lysosomal degradation of cell's' own components.
Eosinophilia
Increased eosinophil production due to IL-5 from mast cells, T cells and macrophages.
NK cells, how are they targeted and what do they do?
Activated by low MHC-1 or activating receptors on target cells. They induce apoptosis on target cells via the extracellular pathway by producing a large amount of cytokines.
Liquefacive necrosis
Inflammatory cells and enzymes liquefy the tissue, hypoxic death of cells in CNS. IF triggered by infection, liquid will contain high amount of neutrophils in the pus, which is eventually removed by phagocytosis leaving a CNS cavity.
Lymphopenia
Decrease in lymphocytes due to some drug therapy (cancerous), AIDs and severe stress.
Lymphocytes T/B cells
Mononuclear, variable in size and shape.
Proliferation
Growing expansion of cells in number and size
Monocyte/macrophage role
Phagocytes, produce pro inflammatory cytokines and present antigen to T cells.
Neutrophilia and causes
Elevated neutrophils Due to: - Infection - Inflammation - Drug induced steroid drugs - leukaemia of myeloid cells, - elevated levels of one type of cell. - promotion of neutrophil production by IL-8.
Monocytosis
increased monocytes - due to prolonged or chronic bacterial infection. Pneumonia or Tb bone marrow cancer
Senescence
Biological aging
Two major reactions of Acute inflammation
Vascular: Vasodilation, increased vascular permeability Cellular: Emigration of leucocytes
Monocyte appearance
Large cells with multilobed nucleus. Differentiate into macrophages when in the tissue. Long lived in tissue.
Karyolysis
Nucleus fades
Hyperplasia
Enlargement of an organ, due to INCREASED NUMBER OF CELLS . Can only occur in LABILE or STABLE tissue (those that undergo mitotic division)
Hypertrophy
Enlargement of an organ or part due to the INCREASE IN CELL SIZE, usually in muscle or organs such as the kidney.
Lean with normal metabolic function
Normal inflammation, metabolic control and vascular function
3 stages of nuclear breakdown
Karyolysis - nucleus fades pyknosis - nucleus becomes shrunken mass karyorrhexis - pyknotic nucleus breaks up.
Coagulative necrosis
Protein denaturation typically caused by ischemia or infarction. In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.
Obese with mild metabolic dysfunction
INCREASED inflammation, DECREASED metabolic control and SAME vascular function.
Caseous necrosis
'cheese like' necrosis e.g. seen in TB.
Neutropenia and causes
Low neutrophils - Marrow suppression drugs - Infections (viral or bacterial) - Genetic
Necrosis
Cell changes due to cell death. Lysis of the cell - burst membrane and spilled cell contents.
Opsonisation
Coating of a particle with a substance that helps it to attach to a phagocytic leukocyte . Important opsonin is C3b of complement and antibody.
Apoptosis
Programmed individual cell death, not involved with inflammation. characteristics include - pyknosis and formation of apoptotic vessels containing nucleus and shit.
Steatosis
Accumulation of Triglycerides - most likely in liver cells. Accumulation of small lipid droplets in cytoplasm.
Infarction
Area of necrosis brought on by obstruction of the circulation.
Lymphocytosis
Increase in lymphocytes Common in acute viral infections or in neonate response to infection.
Dysplasia
Disordered growth, occurs after persistent injury or irritation.
Oedema
Swelling due to build of fluid in the tissue.
Karyorrhexis
Pyknotic nucleus breaks up
Section 2
(50 cards)
Keloid
Too much proud tissue (granulation tissue) or collagen - replaced with scar tissue
Diapedesis
process of vasodilation and increased vascular permeability of the affected areas blood vessels via chemical mediators, Monocytes, neutrophils and endothelial cells become STICKY from secretion of adhesion molecules (SELECTINS AND INTEGRINS) and adhere to the the endothelial cells - MARGINATION. Once adhered, the can move between the endothelial cell gaps - this process alone is called diapedesis. Neutrophils will die via apoptosis after 24-48 hours in the tissue - releasing destructive enzymes into tissue.
What is sequestrum?
Dead bone in osteomyelitis
Clonal Proliferation
Cells that have uncontrolled growth and fail to die. When clone is big enough it can replace normal marrow and infiltrate into other tissues, replacing and destroying normal cells.
Exudate
Due to the pooling of neutrophils, macrophages and protein rich plasma in injured areas (oedema). Globulin is present in selective protein rich exudate.
Two processes of tissue repair
- regeneration of cells of the same type These cells must be labile or stable and must have structural framework. - Replacement by connective tissue: fibrosis or scarring. When cells are permanent (brain and heart) or structural framework has been severely damaged.
What are the 4 mechanisms of action that complement has?
- To split C3 to generate C3a and C3b these then generate... - Opsonise microorganisms - Degranulate mast cells to release inflam and chemotactic mediators e.g. histamine - Assemble the membrane attack complex which causes perforation of target membrane.
Chemotaxis
the act of diapedesis and movement towards the affected area once through the vessel wall.
Erythrocyte Sedimentation rate
Fibrinogen is converted to fibrin which we can measure in the blood. Fibrinogen causes RBCs to stick together.
Fibrinolytic pathway is activated by what?
Plasmin - which has a main function of lysing fibrin clots. Can also cleave c3 to c3a and activate Factor XII.
What is the NK cell killing mechanism?
1. receptors on NK cells bind to surface molecules on target cell. 2. NK cells release PERFORIN which cause transmembrane channels in target membrane -> GRANZYMES enter cell and DNA fragmentation leads to death. OR 3. NK surface molecule Fas ligand binds to target cell surface molecule Fas which leads to apoptosis.
Process of Neutrophil movement
Initiated by TNF-a and IL-1 secretion from activated macrophages at site of infection. 1. Rolling of leukocytes along endothelial wall (Adhesion molecules - selectins are responsible for rolling) 2. Integrin (integrin ligand ICAM 1)adhesion molecules - cause leukocytes to adhere by high affinity to blood vessel wall. 3. Chemokines (mainly IL-8) produced at site of infection enter the vessel and bind to endothelial cells surface. 4. Migration of leukocytes occurs across endothelial cells into tissue - diapedesis - caused by histamine, serotonin and C3a and C3b.
Acute inflammation is initiated and lasts..
Initiated within minutes and lasts around 2-3 days
Does the scar tissue achieve normal strength once healing process has occurred?
NO, the scar only achieves 70-80% strength of normal tissue by 3 months. Never regain 100%
Dendritic cell types of endocytosis
- Phagocytosis - unspecific - Pinocytosis - more specific - smaller amounts - Receptor mediated endocytosis
What mediators stimulate migration and proliferation of fibroblasts and where are they secreted from?
Growth factors - TGF-B, PDGF, EGF, FGF from activated endothelium and macrophages - IL-1 and TNF-a
Involucrum?
New bone in the repair of osteomyelitis
Healing by primary intention vs. secondary intention?
Primary intention - clean incision with line of closure that fills with clotted blood, the dehydration of that tissue and blood result in a scab formation. Secondary intention - large tissue defect ( large gap in epithelium) which results in more inflammation, more granulation tissue - wound contraction due to myofibroblasts and secondary infection is very common with ulcer formation.
Pus contents
Dead tissue Living and dead leukocytes antibodies
The three acute phase proteins
Fibrinogen CRP- 1 Haptoglobin ALL RELEASED BY LIVER DURING INFLAMMATION
Granulation tissue is composed of what and when does it appear in the healing process?
-Pink, soft -Contains new thin walled blood vessels.(Endothelial channels over time differentiate into new blood vessels) -Fibroblasts -Connective tissue matrix (ECM) Appears 3-5 days after injury
Membrane attack complex is composed of what?
C5b links to c7,c8 and c6 with a ring of C9 on the outside. this complex punches a hole into the cell wall of bacteria causing lysis of the cell.
3 ways acute inflammation is regulated
- only occurs when there is tissue injury - Terminated when injurious agent is eliminated as mediators are short lived. - Activation of acute inflam. also triggers anti inflam reactions.
What is acute osteomyelitis?
Infection within the bone marrow cavity
Natural killer cells respond how to MHC class 1?
NK cell activity is inhibited when they recognise their own MHC 1 on target cells.
Adhesion molecules
Selectin and integrin regulated by cytokines released in response to infection or tissue necrosis.
Which pathway ends up with more complement and why?
Classical pathway, because you get a higher yield of the enzyme that chops up C3 and C5 so end up with more complement than the alternative pathway.
Angiogenesis
Formation of new blood vessels - mobilised by EPC being released from bone marrow.
Can stable cells regenerate?
Can go back into cell cycle once it has been stimulated. e.g. liver and kidney. IF they are hurt WITH original connective tissue they can repair. IF NOT they have to be replaced via fibrosis or scarring.
Can permanent/quiescent cells regenerate?
NO, they do not have ability to re enter cell cycle and be replicated. e.g. myocardial fibres in heart and brain cells. No fibroblasts present in CNS.
Bradykinin as a vasoactive mediator facilitates..
Dilation, permeability and pain.
What does the innate immune response involve?
- NK cells - activation of the alternative complement pathway - Phagocytosis - Acute phase proteins NO T OR B cells are involved in innate immunity.
Margination
The adhesion of monocytes and neutrophils to the endothelial wall of a blood vessel as a result of adhesion molecules.
The three phases of scar formation and the time phrames
1. Inflammation ~24 hours 2. Granulation tissue formation, with angiogenesis, fibroblast migration and proliferation and new ECM. ~3-7 days 3. Scar remodelling ~weeks - months - never regain full functionality. Get white hard scar + 3months.
Myeloid stem cells become:
Basophil Neutrophil Eosinophil Monocyte Can also become ethyroid cell - RBC. Are the main cell type associated with acute inflammation.
What are the four stages of tissue repair?
1. Angiogenesis - formation of new blood vessels 2. fibroblast migration and proliferation 3. Deposition of ECM 4.maturation and organisation (remodelling) of scar tissue
Oxinisation
The splitting of C3 and C5 into a and b subtypes for activation of complement system.
What does Factor XII do and how does it get to tissue?
Factor XII triggers both the kinin and coagulation cascades (clotting and fibrinolysis), it triggers this response by diffusing through the blood vessel epithelia as part of the plasma transudate when vessel has increased permeability. Once in the tissue, it is activated on contact with collagen or basement membrane of vessel wall.
Chemical mediators involved with PAIN
Bradykinin and prostaglandins
Chemical mediators involved with HEAT
TNF and IL-1
Chemical mediators involved with Vasodilation
- Histamine - Nitric Oxide - Prostaglandins
C3a and C5a Facilitate what 6 things?
Recruit neutrophils into the site Acute inflammation Vasodilation Chemotaxis Transudation - process of fluid crossing membrane Phagocytosis
In innate immunity, once macrophages have been activated what do they secrete and what does that result in?
TNF-a and Il-1 - Leads to E-selectin secretion (increased adhesion secretion) and ICAM-1 - act on blood vessel wall epithelia. Il-8 - recruits neutrophils
Chemical mediators involved with Leukocyte recruitment, activation and chemotaxis
- Cytokines ( TNF and IL-1) - Chemokines (IL-8) - C3a and C5a
Can labile cells regenerate?
Yes they are always in the cell cycle e.g. gut epithelium and skin. Usually always dying and dividing.
timelines of healing.
Three types of leakage of blood vessels
Normal - plasma proteins stay in vessel Transudate - fluid leakage due to increased hydrostatic pressure and decreased colloid osmotic pressure. Exudate - Fluid and protein leakage
Thrombin as a key mediator of the clotting system does what?
Converts fibrinogen to a fibrin clot and has proinflammatory effects (increased permeability and endothelial cell activation).
Natural killer cells can acquire antibody via what?
CD16 Fc receptors which allow specific antigen recognition.
Chemical mediators involved with increased vascular permeability
- Histamine - serotonin - C3a and C5a
Section 3
(50 cards)
What is atherosclerosis?
Lipid materials acting as a pathogen that is not eliminated causing a chronic inflammation response.
What is Dyslipidemia?
Elevated plasma cholestereol and TG, lower concentrations of HDL-C - contributes to atherosclerotic risk.
Three phases of bone repair and the time frames
Inflammatory phase 1-5 days (first week) Reparative phase - 7 days -few weeks Remodelling phase - long term
What is hypercholesterolemia outcomes?
Increase in cholesterol via LDL - big increase in serum cholesterol - serum TG levels are normal - High atherogenecity
Hypertriacylglyceridemia
Increase in VLDL Normal to slightly elevated sreum cholesterol increased TG serum levels has relative atherogenicity.
Systemic miliary Tb
The organisms spread through the blood system Almost every organ in the body can be seeded Lesions resemble those in the lung
B Cells and T cells produce what?
B cells produce antibody (IgM, IgG, IgA and IgE) T cells divide into CD4 T helper cells which secrete cytokine TH1. TH2, TH17 and Treg. CD8 cytotoxic cells induce apoptosis in target cell.
High levels of ESR, HDL, Ferritin, Homocysteine and blood glucose, monocytes are indicators of what?
Chronic inflammation
What are fatty acids made out of?
Carboxylic acid with an aliphatic chain.
What is the synoviums function
Lines the non-articulating aspects of the joint, secretes synovial fluid which acts as lubricant.
What are foam cells?
Macrophages that have engulfed oxidised LDL. These form fatty streaks in the arterial intima and start off atherosclerosis.
The synovial Knee joint is protected against bone ends grating together by which secretions?
Type II collagen, aggrecan (major proteoglycan - provides hydrated gel structure) and proteoglycans.
Involucrum
The new bone that is laid down beneath the periosteum which entraps the sequestrum causing chronic osteomyelitis.
Define Antigen
Any substance that can bind to an antibody and generate an immune response.
What is osteoarthritis?
A change in the homeostasis of chondrocytes, cartilage is degenerated as synthesis of proteoglycans and collagen are decreased and their degradation increases. This disease leads to fibrillation of cartilage. 1. Fibrillation 2. Eburnation 3. Sclerosis 4. Subchondral cysts 5. Osteophytes.
Miliary pulmonary disease
Organisms drain through lymphatics into the lymphatic ducts, and to right side of heart Miliary lesions may expand and coalesce to yield almost total consolidation of large regions or even whole lobes of the lung
Wound rupture (dehiscence), ulceration (inadequate blood supply - common in diabetics, and infection are all examples of what?
Factors leading to inadequate scar formation.
What are the key components of a normal joint?
1. Cartilage 2. Synovium 3. Supporting ligaments and joint capsule
Which two lipids contribute most to disease?
Triacylglycerols and cholesterol.
What are epitopes?
It is the part of the antigen recognised by the antigen combining site of an antibody or T cell receptor. Conformation is important as it determines the degradation and recognition of the antibody.
What is osteomyelitis?
chronic Inflammation of the bone marrow. starts off as acute due to infection. Usually caused by Staph. Aureus.
What is a callus composed of?
Granulation tissue containing bone or cartilage.
IDL composition
25% TG and 35% cholesterol
What is the primary complex?
when Tb has infected the apex area of the lung and a lymph node - isolated ghon complex +lymph node.
APO E is located on what lipoproteins?
Chylomicrons, remnants, VLDL, HDL, IDL. Acts as LDL receptor ligand
three outcomes of chronic inflammation
-Abscess - via liquefactive necrosis -Persistent inflammation - chronic, due to failure to completely eliminate injury to the tissues. -Healing
What is rheumatoid arthritis?
The pathogen is part of the synovial tissue/cells - destruction of tissue and joints occur from continued pathogen.
Joint immobility via fibrous tissue or bone fusion prevents movement in rheumatoid arthritis is called what?
Ankylosis
Bile acid, sex and adrenal hormones and vitamin D all need what lipid component?
Cholesterol.
sequestrum
Dead bone resulting from either pressure within the marrow cavity or due to loss of the blood supply because of the lifting of the periosteum,
LDL
5% TG and 60% cholesterol
APO B-100 is present on what lipoproteins and has what function?
VLDL, IDL, LDL Acts as LDL receptor ligand.
What are the components of a granuloma?
inside - the silica (foreign body like TB) then layer of macrophages which can form giant cells with multiple nucleus's, then have collagen, granulation tissue, lymphocytes and neutrophils are the outside.
What is rheumatoid arthritis?
The formation of a pannus in the joint which erodes the cartilage and bone, causing joint deformation and pain. treated with steroids, immunosuppressants and physiotherapy.
Chylomicron composition
85% TG and 10% cholesterol
Duration of chronic inflammation?
Weeks
What is psoriasis
Immune response triggers skin to reproduce heavily which builds up outer layers (epidermis and keratin) - the epidermis thickens and blood flow increases causing red skin with grey scales.
Pus oozing into soft tissue in chronic osteomyelitis is called what?
Abscess
VLDL composition
55% TG and 20% cholesterol
Eburnation
The grinding of bone that results in the surface becoming shiny and smooth - like ivory bone.
Hyperlipidaemias
increase in cholesterol and TG only
What are the four major lipids in the body?
1. Cholesterol 2. Phospholipid 3. Fatty acids 4. Triacylglycerol
Abscesses may open onto the skin surface forming what?
A sinus.
HDL
5% TG and 20% cholesterol.
What are triacylglycerols made out of?
Glycerol and 3 fatty acids.
What are phospholipids made out of?
Glycerol, 2 fatty acids and a phosphate group.
Fibrillated cartilage
Cartilage breakdown - edges become frayed and jagged - fibrillation occurs as cartilage is lost over time.
Pannus is made of what?
granulation tissue, proliferation of synovial lining cells and fibrous connective tissue. Macrophages, neutrophils and dendritic cells will also be present.
Wound contraction is most common in what victims and why?
Burn victims, because there is too much wound contraction over a joint so can lose joint function - common in burn victims as healing is accelerated and most skin has been destroyed.
Outline the key stages in atherosclerosis
1. Damage in blood vessel epithelia 2. LDL enters the intima and becomes oxidised. 3. Monocytes enter the wounds and convert to macrophages where the uptake the oxidised LDL. 4. The macrophages become foam cells that either die to release cytokines and cholesterol increasing plasma levels. 5. Cytokines act on smooth muscle cells so that they replicate and proliferate and form the fibrous cap on top of the lipid core from the LDL cholesterol. 6. the plaque/cap can rupture or become weakened and become a thrombus or detach and become an embolism.
Section 4
(16 cards)