BBS2001 Threats and Defence Mechanisms
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| Which leukocytes are myelocytes? are they granular or agranular? | Granular neutrophils, granular basophils, granular eosinophils, agranular monocytes |
| What happens during the platelet plug formation of hemostasis? | Platelets attach to the now exposed collagen fibers. a bridge between the collagen and platelets is formed by the Von Willebrand factor |
| Which leukocytes are lymphocytes? are they granular or agranular? | B and T lymphocytes, both agranular |
| What happens during the platelet plug formation of hemostasis? | Platelets attach to the now exposed collagen fibers. a bridge between the collagen and platelets is formed by the Von Willebrand factor |
| What is the order of most to least abundant leukocytes? | Neutrophils, lymphocytes, monocytes, eosinophils, basophils (never let monkeys eat bananas) |
| What happens during the platelet plug formation of hemostasis? | Platelets attach to the now exposed collagen fibers. a bridge between the collagen and platelets is formed by the Von Willebrand factor |
| Describe the characteristics of platelets | Platelets are called thrombocytes, cell fragments from megakaryocytes, stick to exposed collagen, adhere to it because of the Von Willebrand factor |
| What happens during the platelet plug formation of hemostasis? | Platelets attach to the now exposed collagen fibers. a bridge between the collagen and platelets is formed by the Von Willebrand factor |
| Describe the steps and phases of hemostasis | Step 1: vascular spasm step 2: platelet plug formation step 3: coagulation phase 1: intrinsic and extrinsic pathway to prothrombin activator phase 2: thrombin activation phase 3: fibrin mesh formation |
| Describe the intrinsic pathway of coagulation | Activated by negatively charged surfaces (e.g. platelets) -> factor XII -> factor XI -> factor IX -> factor IX/VIII complex -> factor X |
| Describe the extrinsic pathway of coagulation | Activated by tissue factor released by endothelial cells -> TF/VII complex formed -> factor X |
| Describe the coming together of the intrinsic and extrinsic pathway of coagulation and the formation of ...? | The intrinsic and extrinsic pathway both activate factor X in the end -> factor X activates factor V -> factor X, factor V, calcium ions and platelet factor 3 activate prothrombin activator |
| Describe phase 2 of coagulation | Prothrombin activator transforms prothrombin (factor II) into thrombin |
| Describe phase 3 of coagulation | Thrombin transforms fibrinogen (factor I) into fibrin thrombin and calcium ions together activate factor XIII fibrin and factor XIII form cross-links between the fibrin polymers -> fibrin mesh |
| What are the names of the 13 clotting factors/procoagulants? | Factor I = fibrinogen factor II = prothrombin factor III = tissue factor /phospholipids factor IV = calcium ions factor V = proaccelerin factor VI = (does not exist) factor VII = proconvertin factor VIII = antihemophilic factor (AHF) factor IX = plasma thromboplastin component (PTC) factor X = Stuart factor factor XI = plasma thromboplastin antecedent (PTA) factor XII = Hageman factor factor XIII = fibrin stabilizing factor (FSF) |
| What happens during vasular spasm of hemostasis? | The break in the blood vessel causes the smooth muscle to vasoconstrict. this is because of the local pain receptors reflex, the damage to the smooth muscle and the chemicals that are released by the broken endothelial cells and platelets |
| What happens during the platelet plug formation of hemostasis? | Platelets attach to the now exposed collagen fibers a bridge between the collagen and platelets is formed by the Von Willebrand factor platelets release chemicals (ADP, serotonin, tromboxane A) that attract more platelets |
| What are the cardinal signs of inflammation and how/why do they occur? | Heat + redness -> vasodilation of arterioles, more blood to injury site pain, swelling and possible temporary loss of function -> increased capillary permeability, fluid leaks out of them into tissues |
| What are the steps of phagocyte extravasation? | 1. leukocytosis 2. rolling adhesion 3. margination/tight binding 4. diapedesis 5. chemotaxis/migration |
| What happens during leukocytosis of phagocyte extravasation? | Broken tissue sends out leukocytosis-inducing factors, neutrophils migrate into the bloodstream and increase in concentration, vasodilation happens, leukocytes closer to the endothelial cells |
| What happens during rolling adhesion of phagocyte extravasation? | Histamine (released by mast cells), TNF-α and LPS cause the release of Weibel-Palade bodies, P-selectin appears on the endothelium. TNF-α and LPS also cause the appearance of E-selectin. P- and E-selectin bind loosely to the leukocytes on the Sialyl-LewisX glycoproteins. the leukocytes roll along the endothelium. |
| What happens during margination/tight binding of phagocyte extravasation? | A chemokine binds to its receptor on the leukocyte, which causes a conformation change of the leukocyte integrins. this increases the adhesiveness of the leukocyte. endothelial cells release intracellular adhesion molecules (ICAMs), ICAMs bind the leukocyte tightly to the endothelium. |
| What happens during diapedesis of phagocyte extravasation? | The leukocytes flatten and squeeze in between the endothelial cells as a result of chemical signals. the basement membrane is broken down by enzymes that digest extracellular matrix molecules. |
| What happens during chemotaxis/migration of phagocyte extravasation? | The leukocytes are in the tissue space and follow the chemical trail to the injury (positive chemotaxis) |
| What is the difference in composition between venous and arterial thrombi? | Venous thrombi: mostly fibrin and erythrocytes, some platelets arterial thrombi: mostly platelets in the core |
| What is Virchow's triad and what does it compose of? | Virchow's triad are the three factors that can lead to venous thrombosis, they are: hemodynamic changes (stasis), endothelial wall injury and hypercoagulation |
| What do hemodynamic changes in Virchow's triad mean? and when does it happen? | Turbulence (disorganized blood flow) and stasis (static pockets of blood) it happens after long periods of inactivity of the skeletal muscle pump (long flights, bed rest) and during pregnancy |
| What does hypercoagulation in Virchow's triad mean? and when does it happen? | Hypercoagulation is the increased amount of clotting factors it can happend during surgery (endothelial damage), birth control medication and genetics |
| What could cause damage to the endothelial lining (Virchow's triad)? | Infection, chronic inflammation, toxins like tobacco smoke, hypertension or shear stress |
| What is the difference between venous and arterial thrombi regarding embolization | Venous thrombi: only a part/tail of the thrombus becomes an embolus, can become a pulmonary embolism or cause an embolic stroke in the brain arterial thrombi: often the entire thrombus becomes an embolus, can effext any organ |
| What is the cause of arterial thrombosis? | Often atherosclerosis, a plaque that ruptures and to which platelets adhere |
| What drugs/structures can be used to treat venous thrombosis? | Heparin: increases the activity of antithrombin, increasing the inhibition of factor Xa and thrombin vitamin K antagonists (warfarin): inhibition of vitamin K unables it to modify a lot of coagulation factors, less clotting as a result fibrinolysis (recombinant tPA): tPA will turn plasminogen into plasmin and plasmin will digest the clots. dabigatran, lepirudin, desirudin: direct inhibitors of either thrombin or factor Xa, no fibrin mesh formed. |
| What drugs/structures can be used to treat arterial thrombosis? | Aspirin: inhibits cyclooxygenase, prevents autofeedback mechanism that amplifies platelet activation ADP-receptor antagonist (clopidogrel): inhibits ADP receptor, ADP cannot bind, less platelets will be attracted. PAR1 inhibition: thrombin cannot bind to its receptor, cannot amplify the cascade. receptor integrin alpha 2b beta 3 inhibition: reduces platelet aggregation by inhibiting binding of platelets to fibrinogen |
| What step in hemostasis should treatments target in both venous and arterial thrombosis? | Venous thrombosis: step 3; coagulation cascade arterial thrombosis: step 2; platelet plug formation |
| How can bacteria be classified? | By macroscopic and microscopic appearance, characteristic growth and metabolic properties, antigenicity and genotype biggest distinction is between gram-negative and gram-positive bacteria |
| How does the gram staining work? | 1. bacteria are heated and dried on a slide 2. they are stained with crystal violet 3. excess stain is removed by acetone-based decolorizer and water 4. a red counter stain called safranin is used |
| What is the difference between gram-positive and gram-negative bacteria? | Gram-positive bacteria: thick, cross-linked cell wall composed of peptidoglycan, only consist of peptidoglycan and cytoplasmic membrane, contain many proteins and acids, stain purple gram-negative bacteria: consist of outer membrane, periplasmic space with some peptidoglycan, cytoplasmic membrane. contain endotoxin, stain red becasue of the thin layer |
| What is serotyping? | Identifying differences between bacteria species by using antibodies to detect their characteristic antigens |
| What do bacteria compose of? | Cytoplasm, cytoplasmic membrane, cell wall, chromosomes, plasmids, 70S ribosomes, flagella, fimbriae not always; capsules, outer membrane, periplasmic space |
| What proteins/structures can be found in gram-positive and gram-negative bacteria? | Gram-positive bacteria: much peptidoglycan (can be degraded by lysozyme), proteins, teichoic and lipoteichoic acids, polysaccharides gram-negative bacteria: very little peptidoglycan, transport systems for iron, proteins, surgars, enzymes, phospholipids, endotoxin (LPS) |
| What are the mechanical barriers of the body? and what are the chemical ones? | Mechanical: skin (keratin), mucus membranes and nostril hairs chemical: acid (skin), hydrochloric acid (stomach), enzymes, mucin, defensins, other chemicals e.g. dermcidin in sweat |
| What are the functions of the innate immune system? | - recruiting immune cells to the site of infection - activation of the complement cascade to identify bacteria - identification and removal of foreign substances - activation of the adaptive immune system - acting as a physical and chemical barrier to pathogens |
| What cells are involved in the innate immune system? | The non-specific cells; neutrophils, mast cells, basophils, eosinophils, macrophages |
| What do neutrophils do in response to an infection? | They fight against bacteria and fungi: their receptors (e.g. scavenger, opsonin) bind to the microbes directly, they promote phagocytosis. their granules also contain antimicrobial proteins and can produce reactive oxygen species (ROS) |
| What do mast cells and basophils do in response to an infection and where are they present? | They are similar to each other in function; they bind IgE, complement and microbial products. they also release histamine and cytokines as part of the inflammatory response. mast cells can be found in the skin, muco-epithelial tissue and the lining of the small blood vessels and nerves. the basophils circulate in the blood. |
| What do eosinophils do in response to an infection and where are they present? | They circulate in the blood and function in antiparasitic responses |
| What do macrophages do in response to an infection and where are they present? | They circulate in the blood, but when there's an infection they migrate into the tissues. they can be subdivided into M1 and M2 macrophages M2: remove debris and promote tissue repair M1: kill phagocytosed bacteria, produce ROS, nitric oxide and enzymes, attract neutrophils, NK cells and activated T cells by producing chemokines |
| What do PAMPs and DAMPs do and how do they work? | They notify the body that there is an infection. PAMPs (pathogen associated molecular patterns) do this by a signal that is released by the pathogen and DAMPs (damage associated molecular patterns) do this by damage that is done to the tissue. the body receives these signals through special receptors; pattern recognition receptors (PRRs) |
| What are the steps of phagocytosis? | 1. attachment; mediated by cell-surface, fibronectin and opsonin receptors 2. internalization; part of the plasma membrane around the pathogen to form a phagocytic vesicle 3. digestion; vesicle fuses with primary lysosomes and become phagolysosomes |
| What happens during an oxidative burst? | It starts during phagocytosis; 1. enzymes in the phagolysosomes are activated 2. one of them, phagocyte oxidase, converts oxygen into superoxide anion and free radicals (ROS), which are toxins 3. inducible nitric oxide synthase converts arginine into nitric oxide, which kills bacteria |
| What are the pathways of the complement cascade and where do they come together? | Alternate/properdin pathway, lectin pathway and classical pathway. they come together with the production of component C3. |
| What is the end product of the complement cascade and what does it do? | The membrane attack complex (MAC), also called lytic unit. it kills infected cells by drilling a hole in their cell membrane, which leads to apoptosis or hypotonic lysis of the cell. |
| What are the PRRs and are they intracellular or extracellular? | TLR -> intracellular and extracellular NLR -> intracellular CLR -> extracellular RLR -> intracellular |
| What do TLR4, TLR5, TLR9, NOD-1 and NOD-2 and NLRP3 recognise respectively? | TLR4 and NLRP3-> LPS TLR5 -> bacterial flagella TLR9 -> bacterial unmethylated CpG DNA NOD-1 and NOD-2 -> bacterial peptidoglycan NLRP3 -> changes in cytosol and forms inflammasome |
| What are the three outcomes of the complement system and what components are involved? | Opsonisation -> increases phagocytosis (C3b) anaphylatoxin -> induce inflammation (C4a, C3a, C5a) lytic pathway -> formation of MAC, lysis of pathogens (C5b, C6, C7, C8, C9) |
| What are the different sizes of PMs and where to they come from? | PM10 (thoracic) -> construction sites, mining sites, paved roads, farming PM2.5 (fine) -> forest fires, volcanos, coal-powered power-stations, factories PM0.1 (ultrafine) -> man-made e.g. cosmetics |
| What do DEPs compose of and how are they generated? | Diesel exhaust particles can be found in diesel exhaust along with gases, it consists of a carbon core with metal and organic compounds on the surface, they can form aggregates. they are generated with the incomplete combustion of fuel. |
| Which PMs get where in the lungs when inhaled? | PM10 -> do not get into the lungs, are removed/eliminated in the trachea PM2.5 -> get to the alveoli PM0.1 -> get to the alveoli and can be diffused into the blood stream |
| How do PMs activate the local inflammatory response? | 1. the PMs are sensed by PRRs 2. the alveolar macrophages release TNF-alpha, IL-1beta, IL-6, IL-8 and granulocyte macrophage colony-stimulating factor (GM-CSF) 3. macrophages can become antigen-presenting cells 4. alveolar and airway epithelial cells are stimulated to produce chemokines |
| How does the local inflammatory response of the PMs become the systemic inflammatory response? | 1. the macrophages produce granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-1beta, which both stimulate the leukocyte production and release from the bone marrow 2. the macrophages also produce IL-6, which stimulate the liver hepatocytes, leading to a production of C-reactive protein, fibrinogen and antiproteases. it also increases the production of platelets. |
| What are the reactive oxygen species? and are they radicals or non-radicals | Radicals: superoxide, hydroxyl, peroxyl, alloxyl non-radicals: hydrogen peroxide, hypochlorus acid, ozone, singlet oxygen |
| How are hydroxyl radicals generated? | Fenton reaction: hydrogen peroxide reacts with iron or copper (Fe2+ + H2O2 →Fe3+ + •OH + OH−) Haber-Weiss reaction; hydrogen peroxide reacts with superoxide (O2•−+ H2O2 → O2 + •OH + OH−) |
| What defense mechanism protects the body against ROS? | Antioxidants, they donate an electron to the radicals to neutralize them |
| What are the most important enzyme antioxidants and what do they do? | Catalase: converts hydrogen peroxide into water and oxygen 2 H2O2 → 2 H2O + O2 superoxide dismutase ROOH + 2 GSH → GSSG + H2O + ROH glutathione peroxidase: converts superoxide into hydrogen peroxide O2 - + O2 - + 2H+ → H2O2 + O2 |
| What are the results of oxidative stress? | It can damage cell structures like DNA, cell membranes, proteins, lipids, lipoproteins and it can cause many types of diseases (cardiovascular, renal, neurological, respiratory) |
| What are the different classes of antibiotics? | Beta lacatams (target cell wall) penicillins cephalosporins, cephamycin carbapenems monobactams target protein synthesis aminoglycosides macrolides target nucleic acid synthesis quinolones antimetabolites |
| What is the differences between penicillins and cephalosporins? | The beta-lactam ring of cephalosporins is fused with a dihydrothiazine ring cephalosporins have a wider spectrum than penicillins |
| How do quinolones work? | They target nucleic acid synthesis by inhibiting topoisomerase type II for gram-negative bacteria and topoisomerase type IV for gram-positive bacteria. this prevents DNA replication, recombination and repair. |
| How do antimetabolites work? | They target nucleic acid synthesis by competing with the enzyme PABA, which is needed for the production of folic acid. because of this inhibition purines and pyrimidines cannot be made |
| How do aminoglycosides work? | They target protein synthesis by binding to the 30S subunit of the ribosome. this creates the wrong proteins causing cell death |
| How do macrolides work? | They target protein synthesis by binding to the 23S ribosomal RNA of the 50S ribosome. this blocks peptide elongation. this is a reversible mechanism |
| How do the beta-lactams work? | They target the cell wall synthesis by binding to the penicillin-binding proteins, which inhibits the assembly of peptidoglycan. this causes lysis and cell death |
| Which antibiotics are bactericidal and which ones are bacteriostatic? | Bactericidal: aminoglycosides, beta-lactams, bacteriostatic: macrolides |
| What is the difference between penicillin G and V? | Penicillin G is unstable in gastric acid and is thus administered intravenously penicillin V is more resistant to gastric acid and is administered orally |
| Why do penicillins work better on gram-positive than gram-negative bacteria? | The gram-negative bacteria have an outer membrane that the penicillins have to cross before they can do their job. this crossing depends on if the antibiotic fits through the pores of the bacteria. the gram-positive bacteria do not have this membrane |
| What is the difference between cephalosporins and cephamycins? | Cephalosporins contain sulfer in their dihydrothiazine ring, while cephamycins have oxygen located there |
| What do the different spectrums tell you about cephalosporins? | The narrow spectrum cephalosporins are the antibiotics that were first found and that are not that effective to a lot of bacteria. the more you move up in spectrum (expanded, broad, extended) the more active the antibiotics are to other bacteria. the antibiotics in the broad spectrum can pass the blood-brain barrier and the ones in the extended spectrum can pass the outer membrane more easily. |
| How is the peptidoglycan of the cell wall synthesized? | 1. the precursors are synthesised and activated in the cell 2. the acetylglucosamine and acetylmuramic acid are attached to bactoprenol 3. bactoprenol is transferred to the other side of the cell wall 4. peptidoglycan is extended; transpeptidases cross-link the peptidoglycan and D-carboxypeptidases remove unreacted D-alanines |
| What does LPS compose of and in what order? (from proximal to distal of the cell) | 1. lipid A 2. core polysaccharide 3. O antigen the bacteria is recognized by its O antigen |
| How does bacterial resistance develop for each antibiotic? | Beta-lactams: decreased concentration of antibiotic at the target, decreased binding to PBP, hydrolysis by beta-lactamases aminoglycosides: modification of the antibiotic, mutation of the ribosome, decreased uptake of antibiotic in the cell, increased efflux quinolones: chromosomal mutations, increased efflux, membrane permeability mutation antimetabolites: changes to the cell membrane |
| What are the four general mechanisms for developing resistance against antibiotics for bacteria? | Target modification efflux immunity (antibiotics bound to other proteins so they can't bind their target) enzyme catalyze destruction (enzyme destroys the antibiotic) |
| What are the four classes of beta-lactamases? | Class A: SHV-1, TEM-s and ESBLs class B: zinc dependent metalloenzymes class C: mainly cephalosporinases class D: mainly penicillinases |
| What is the function of beta-lactamases? | They work against beta-lactam antibiotics by hydrolyzing them, meaning the addition of a water molecule. this causes the beta-lactam to fall apart in small pieces. |
| What types of ESBLs are there and how are they formed? | TEM: formed by point mutation (in TEM-1 or TEM-2) SHV: formed by point mutation CTX-M: formed by horizontal gene transfer |
| How is bacterial resistance tested? | Disc diffusion test: bacteria are put on an agar plate, antibiotic is applied and discs are incubated, looked at the zone of inhibition broth dilution: bacteria is mixed with media and compared to other tubes to determine the minimum inhibitory concentration (MIC) |
| What is the breakpoint and minimum inhibitory concentration? | Breakpoint: chosen concentration of the antibiotic which defines whether the bacteria is susceptible or resistant to the antibiotic minimum inhibitory concentration: lowest concentration of the antibiotic that inhibits the growth of the bacteria bacteria is resistant when MIC is above the breakpoint bacteria is susceptible when MIC is equal to or below the breakpoint |
| What is horizontal gene transfer and what are the different types? | Horizontal gene transfer is the transmission of genes between two already existing cells. this can be done by conjugation, transduction, transformation |
| How does transduction work? | The transfer of genes is conducted by viruses; bacteriophages. 1. the bacteriophage attaches and infects the bacteria with its own genome. 2. the viral DNA is then integrated in the bacterial genome. 3. when the viral DNA is removed again, it might take some bacterial DNA with it. 4. the virus can infect other bacteria, with that piece of bacterial DNA. |
| How does conjugation work? | 1. the donor bacteria contains the fertility factor on the F plasmid 2. the donor forms an extending structure towards the recipient; the sex pilus 3. one of the strands of the F plasmid is transferred 4. replication of the F plasmid takes place in both bacteria |
| How does transformation work? | It is the uptake of free genetic material by competent bacteria |
| What is plasmid incompatibility? | Two plasmids with the same replication mechanism can't be present in the same bacteria |
| What is the function of transposons? | They are jumping genes that can transfer DNA from one position in the bacterial genome to another |
| What are the three types of transposons? | Insertion sequences: simple transposons, only contain the minimal genetic information needed for its own transfer composite transposons: complex transposons, contain a central region with insertion sequences flanking it, contain genes for antibiotic resistance etc. non-composite transposons: complex transposons, contain genes for antibiotic resistance etc. but have no insertion sequences flanking them |
| What is the function and composition of integrons? | Integrons promote expression of certain genes by shuffling them they compose of an Intl gene, a recombination site where gene cassettes can be inserted and a promotor. |
| What are the differences between commensal, primary and opportunistic bacteria/pathogens? | Commensal bacteria: not pathogenic, aid in digestion, produce vitamins, activate immune response primary pathogens: bacteria that will always cause disease opportunistic pathogens: bacteria that will only cause disease when the host's immune system is weak |
| What are the virulence factors? | Capsule, biofilm, adherence, invasion, by-products of growth, toxins, degradative enzymes, cytotoxic proteins, endotoxin, superantigen, intracellular growth, resistance to antibiotics, evasion of phagocytosis and immune clearance, induction of excess inflammation |
| How do bacteria adhere to the body surfaces? | They use adhesins on the tips of their fimbriae to bind to the sugars of the surface, these adhesins are also called lectins. they can also form a biofilm when there are enough bacteria; quorum. this is determined by quorum sensing |
| How do bacteria destroy tissues? | They have toxins that can be released and become exotoxins. most exotoxins have an A and B subunit (B for binding and A for injury (action)). they also have endotoxins, which are released when the cell lyses. they have superantigens that activate T cells without there being an antigen. this promotes shock, life-threatening fever etc. |
| What does EHEC stand for and what are its adhesins and toxins? | EHEC -> enterohemorrhagic E. coli adhesins: bundle-forming pili (BFP), intimins toxins: Shiga toxins 1 and 2, verotoxin |
| What does EPEC stand for and what are its adhesins and toxins? | EPEC -> enteropathogenic E. coli adhesins: bundle-forming pili (BFP), intimins toxins: / |