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1. 1Select all of the 5 cardinal signs for inflammation

   1. ARedness
   2. BWarmth (heat)
   3. CSwelling
   4. DPain
   5. ELoss of function
   6. FPus
2. 2Steps of inflammation

   1. ABradykinin = Vasodilation, Hyperalgesia, increased vascular permeability, SM contraction
   2. BBradykinin = Vasodilation, increase vascular permeability, cellular infiltation
3. 3What is the purpose of inflammation - Pick all 3

   1. AEliminate/ remove damaging agent
   2. BPrevent further cell damage
   3. CClean up tissue to allow for healing
   4. DDestroy tissue components
   5. EFor the cell to brathe
4. 4What are the two phases of inflammation

   1. AVascular Phase & Cellular Phase
   2. BCellular Phase & Acute Phase
   3. CChronic Phase & Acute Phase
5. 5Chemical mediators of inflammation Roles
   Prostaglandins

   1. AVasodilation, altered platlet function, Fever
   2. BIncreased vascular permeability, contraction of SM
6. 6Chemical mediators of inflammation
   Bradykinin

   1. AVasodilation, increased vascular permeability, contraction of SM
   2. BChemotaxis, Platlet aggregation
7. 7Chemical mediators of inflammation
   Leukotrienes

   1. ABronchoconstriction, increased vascular permeability, chemotaxis
   2. Bfever, uterine contraction, vasodilation
8. 8Chemical mediators of inflammation
   Histamine

   1. AVasodilation, increased vascular permeability, contraction of SM
   2. BPromotes PG action, vasoconstriction
9. 9Chemical mediators of inflammation
   Cytokines

   1. APeptide secretions from inflammatory and blood cells, communication between inflammatory cells
   2. BFever, contraction, PG action
10. 10Define Exudate

    1. AFluid that moves out of blood vessels during inflammation and accumulates in the tissue
    2. BFluid that transports blood components

11. 11Types of Exudate

    1. ASerous, Fibrinous, Purulent, Haemorrhagic
    2. BSerous, Fribin, Purulent, Haemaglobin
12. 12Define Serous (TYPE OF EXUDATE)

    1. AWatery with low protein content, Mild response, common in skin blister
    2. BWatery with high protein content, severe response
13. 13Define Fibrinouse ( TYPE OF EXUDATE)

    1. AFibrin formation and high plasma protein content
    2. BMay inhibit healing process - very viscous and sticky
    3. CWatery with low protein content
    4. DMay lead to adhension - adjacent tissue layers adhering
14. 14Define Purulent (TYPE OF EXUDATE)

    1. AContains pus- cellular debris and living and dead cells
    2. BUsually asscoaiated with inflammation caused by bacteria infection
    3. CAbscess - Large volumes of pus
    4. DMay reduce effectiveness of antimicrobial agents
    5. EMild response
15. 15Define Haemorrhagic (TYPES OF EXUDATE)

    1. AContains red blood cells
    2. BIndicative of signicant injury to blood vessles
    3. CMild response
    4. DCommon skin blister
16. 16Define Acute Inflammation

    1. AStarts rapidly (rapid onset) is a short-term process occurring in response to tissue injury, usually appearing within minutes or hours.
    2. BTwo weeks or more appearing withing minutes or hours
17. 17Define Chronic inflammation

    1. Arefers to a prolonged inflammatory response that involves a progressive change in the type of cells present at the site of inflammation. It is characterized by the simultaneous destruction and repair of the tissue from the inflammatory process.
    2. BLast for two weeks max
18. 18Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Asprin

    1. ACOX-1 & COX-2 inhibitor (analgesic, anti-pyretic, anti-inflammatory, anti-platelet)
    2. Bsteriodal anti-inflammatory drugs
19. 19Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Ibuprofen

    1. ACOX-1 & COX-2 inhibitor (analgesic, anti-pyretic, and-inflammatory)
    2. BPotentially a COX-3
20. 20Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Paracetamol

    1. APotentially a COX-3 inhibitor (analgesic, anti-pyretic, poor anti-inflammaotry
    2. BCOX-1 & COX-2 inhibtor
21. 21Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Celecoxib

    1. ACOX-2 inhibitor (analgesic, anti-inflammatory, potentially increase platlet aggregation)
    2. BPotentially a COX-3 inhibitor
22. 22Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Glucocorticoids

    1. ASteriodal anti-inflammatory drugs (adrenal cortex)
    2. BCox-2 inhibtor
23. 23Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Hydrocortisione (cortisol)

    1. Adecrease prostaglandin, decrease pro-inflammatory transcriptions (e.g cytokines)
    2. Bprostaglandin production
24. 24Anti-Inflammatory Medications (NSAIDS & Glucocorticosteroids)
    Cortisone

    1. AProstaglandin production, decrease pro-inflammatory transcritpion (e.g. cytokines)
    2. BCOX-1 & COX-2 inhibtor
25. 25Define wound healing

    1. AThe process of healing and repairs is the restoration of the damaged functional tissues cells (parenchyma) and to re-establish the framework of tissue through scar formation
    2. Bobjective is to stop the bleeding
26. 26Stages of healing

    1. AHealing: replacement of lost functional tissue cells
    2. BRepari: Scar formation to re-establish framework of tissue
    3. CHemostasis: rebuild the body process
27. 27Process of wound healing

    1. AInflammatory Phase, Proliferative Phase, Remoldeling/Maturation Phase
    2. BProliferative phase
    3. CRemoldeling/Maturation Phase
    4. DHemostasis
28. 28Types of wound healing

    1. AFirst intention
    2. BSecond intention
    3. CPrimary wound closure
29. 29Factors that slow healing

    1. AInfection: microorganisms damage cells, imduce excessive accumulation od exudate in tissue
    2. BMovement: New tissue lack tensile strength - movement can disrupt the integrity of newly tissue
    3. CPoor nutrition supply: newly forming tissue has increased metabolic demands- it requires higher levers of glucose, proteins and nutirents to sustain growth
    4. DPoor blood flow: inadequate blood flow cannot sustain the supply of oxygen for growth and faciliate waste removal
    5. EVitamins: can reduce the healing process
30. 30Bacteria: Unicellular organisms that do not require living tissue to survive
    
    Methods of categorising

    1. ABacilli - Rod Shaped organisms
    2. BCocci - Spherical forms (diplococci, Streptococci, Staphylococci)
    3. CBudding and appendaged bacteria (hypha and stalk)
    4. DCIrcle
31. 31How are Bacteria (Prokaryote) cells differ from Human (Eukaryote) cells?

    1. ABacteria: Does not contain a nucleus. Not linear, bundled into chromosomes, circular, doubled strandled. Nucleoid, Thick protective cell wall is presenting covering the whole cell
    2. BHuman: Multiple chromosomes and linear, Membrane-bound organelles. Doubles and stranded. DNA sits with a nucleus which is a membrane that encloses or contains genetic material = true nucleous.
32. 32Gram-positive are bacteria that give a positive result in the gram stain test - Thick peptidoglycan layer cell wall. Retains crystal violent. More susceptible to antibodies

    1. ARichtig
    2. BFalsch
33. 33Gram-negative = are a group of bacteria that do not retain the crystal violent used in the gram staining method of bacterial differentiation. Characterized by their cell envelopes, which are composed if a this peptidoglycan cell wall sandwiched between an inner cytoplamic cell membrane and a bacterial outer mebrane. More resistant to antibiotics

    1. ARichtig
    2. BFalsch
34. 34Difference between gram + and gram - bacteria
    
    This is due to the difference in the structure of their bacterial cell wall. Gram-positive bacteria do not have an outer cell membrane found in Gram-negative bacteria. The cell wall of Gram-positive bacteria is high in peptidoglycan which is responsible for retaining the crystal violet dye.

    1. ARichtig
    2. BFalsch
35. 35Antibiotics: Aminoglycoside

    1. ANegative gram
    2. BProtein synthesis​ 30's
    3. CStreptomycin
36. 36Gentamicin is a bactericidal antibiotic that works by binding the 30s subunit of the bacterial ribosome, negatively impacting rotein sythesis

    1. ARichtig
    2. BFalsch
37. 37Streptomycin is an antibiotic that acts by binding tto the 30s ribosomal subunit of susceptible organism and disrupting the initiation in protein sytheses

    1. ARichtig
    2. BFalsch
38. 38Cephalosporins Antibitoic

    1. APositive and Negative Gram
    2. BCell wall synthesis
    3. CCephalothin
39. 39Penicillin

    1. APositive Gram
    2. BCell wall synthesis
    3. CPenicillin and amoxicillin
40. 40Tetracycline Antibiotic

    1. APositive & Negative Gram
    2. BProtein synthesis 30s
    3. CTetracycline
41. 41Quinolones/ Fluro Qunilones Antibiotics

    1. APositive and negative gram
    2. BInhibitions of DNA replication
    3. CCiprofloxacin
42. 42Macrolides Antibiotics

    1. APostive Gram
    2. BProtein synthesis 50s
    3. CErythromycin
43. 43Sulphonamides Antibiotic

    1. APositive and Negative Gram
    2. BSynthesis of Folate
    3. CSulfamethoxazole & trimethoprim
44. 44Glycoproteins Antibiotic

    1. APostive Gram
    2. BCell wall Synthesis
    3. CVancomycin
45. 45The common causes of resistance of antibiotics are when human over prescribe antibitics, When people dont take antibiotics as directed.
    
    Some bacteria are naturally resistant to some antibiotics: this is known as innate resistance

    1. ARichtig
    2. BFalsch
46. 46Major concern with antibiotcs use is the Efficacy, Allergic reaction and Resistance e.g MRSA

    1. ARichtig
    2. BFalsch
47. 47TYPES OF OPPORTUNISTIC INFECTIONS AFTER USING ANTIBIOTICS

    1. ASecondary Infection = Infection cause by pathogen
    2. BViral, bacterial, fungal OR PARASITIC INFECTIONS. they occur in patients with a weakned or compromised immune system.
48. 48Physiology of Infection

    1. AIncubation period: the time between entry of the organism into the body and appearance of clinical signs of disease.
       
       Refers to the time between pathogen entry and first appearance of clinical manifestation peak
    2. BProdromal period: Fatigue, loss of appetit, headache. Nonspecific - " coming down with something"
    3. CAcute Period: Infectious disease develops fully. Multiples at high levels, reached target tissue, greatest toxicity during this stage
    4. DConcalescent Period: Recovery period - time when acute symptoms or illness disapper
49. 49Is it true that
    
    Innate - is a non specific response mechanism
    
    Adaptive - Which is a specific defence mechanism that responds​ to a potentially harmful substance

    1. ARichtig
    2. BFalsch
50. 50Explain different divisions of immune systems

    1. AInnate = Monocytes, Eosinophil, Neutrophil, Basophil, NK Cell
       Adoptive = T cell, B cell, helper T cell, Cytotoxic T cell
       Both = Macrophages and Dendritic cell
    2. BAdoptive = T cell, B cell, helper T cell, Cytotoxix T cell
    3. CBoth = Macrophages and Dendritic cell
51. 51Physiology of these cells
    Monocytes are WBC: that migrates from the blood into tissues to become macrophages

    1. ARichtig
    2. BFalsch
52. 52Physiology of these cells
    Eosinophil is a WBC: participates in allergic responses and defence against parasites

    1. ARichtig
    2. BFalsch
53. 53Physiology of these cells
    Neutrophil is a WBC for phagocytosis: innate defence; active in inflammation

    1. ARichtig
    2. BFalsch
54. 54Physiology of these cells
    Basophil is a WBC: binds IGE, release histamines

    1. ARichtig
    2. BFalsch
55. 55Physiology of these cells
    NK Cell destroyes foreign cells, veins infected cells and cancer cells

    1. ARichtig
    2. BFalsch
56. 56Physiology of these cells
    T cell specialized lymphocytes produced by the bone marrow and matured in thymus, which is responsible for cell-mediated immunity

    1. ARichtig
    2. BFalsch
57. 57Physiology of these cells
    B cell Specialised lymphocytes produced and mature bone marrow, and precursor to plamsa cells which produced antibodies or memory cells

    1. ARichtig
    2. BFalsch
58. 58 Physiology of these cells
    Helper T cell - Activate B and T cells: control or limit specific immune response

    1. ARichtig
    2. BFalsch
59. 59Physiology of these cells
    Cytotoxic T cell destroys antigens, cancer cells and virus cells

    1. ARichtig
    2. BFalsch
60. 60Physiology of these cells
    Macrophages - phagocytes: process and present antigens to lymphocytes for immune

    1. ARichtig
    2. BFalsch
61. 61Physiology of these cells
    Dendritic cell - antigen presenting cell that stimulate immune response

    1. ARichtig
    2. BFalsch
62. 62Autoimmune disease is a disorder resulting from an overactive immune system that fails to recognise itself
    
    caused by an overactive immune systems that occur when an excessive and inappropriate inflammatory​ reaction occurs against self-antigens

    1. ARichtig
    2. BFalsch
63. 63Name of Autoimmune disease

    1. AType 1 diabetes
    2. BGraves disease
    3. CHashimotos disease
    4. DMultiple sclerosis
    5. ERhematoid arthrisits
64. 64What are the four types of hypersensitivity​ reaction

    1. AType 1: Allergice Reaction
    2. BType 2: cytotoxic Hypersentivity
    3. CType 3: Immune complex Hypersenitivty
    4. DType 4: Cell-mediated or Delayed Hypersensitivity
65. 65What are the four types of hypersensitivity reaction
    Type 1: Allergic Reaction
    
    Free antigens cross-link the IGE on mast cells and basophils, which cause a release of vasoactive biomolecule.
    
    Examples: Hay fever, anaphylaxis
    Effects: Immediate inflammation (redness, swelling, blister vesicles and pruritus

    1. ARichtig
    2. BFalsch
66. 66What are the four types of hypersensitivity reaction
    Type 2 Cytotoxic Hypersensitivity
    
    Antibody (IGM OR IGG) binds to antigen on a target cell, which is actually a host cell that is perceived by the immune system as foreign, leading to cellular destruction.
    
    Examples: Graves disease, ABO blood incompatibility
    Effects: Cell lysis and phagocytosis

    1. ARichtig
    2. BFalsch
67. 67What are the four types of hypersensitivity reaction
    Type 3: Immune Complex Hypersensitivity
    
    Antibody (IGG) binds to soluble antigen, forming a circulating immune complex. This is often deposited in the vessel walls of the joints and kidneys, initiating a local inflammatory reaction
    
    Example: Rheumatoid Arthritis, SLE (Systemic Lupus Erythematosus
    Effects: Inflammation, Vasculitis

    1. ARichtig
    2. BFalsch
68. 68What are the four types of hypersensitivity reaction
    Type 4: Cell-mediated or delayed Hypersensitivity
    
    Helper T cells are activated by an antigen presenting cell. When the antigen is presented again in the future the memory helper T cells will activate macrophages and cause an inflammatory response
    
    Effects: Delayed inflammation, serous vesicles
    Example: Contact dermatitiis, transplant rejection, IBD, Diabtetes type 1

    1. ARichtig
    2. BFalsch
69. 69Types of vaccines

    1. ALive attenuated: Weakened virus -> measules, mumps, chickenpos
    2. BInactivated virus: Pathogen is destroyed -> influenza
    3. CSubunit Vaccines: Epitopes (parts of proteins) -> Hep.B
    4. DTaxoid Vaccines: Bacteria inactivated w/ formalin -> diphtheria, tetnus
70. 70Vaccines work by priming the adaptive immune response to the antigens of a particular pathogen

    1. ARichtig
    2. BFalsch
71. 71Vaccines work by an inactivated or weakened disease-cauing microorganism (virus or bacteria) is introduced to the immune system. Immune cells of the adaptive system recognise a potential threat and elicit an immune response - comprising of the production of antibodies and memory cells. Future encounters with the same disease-causing microorganism will be target and destroyed.

    1. ARichtig
    2. BFalsch
72. 72Glucocorticosteroids: steroid hormone which exert anti-inflammatory actions, that is; they stop inflammation in the body
    
    also called glucocorticoids, corticosteroids or steroids most effect anti-inflammatory drugs.

    1. ARichtig
    2. BFalsch

Beschreibung

Quiz am -, erstellt von Alana Mcdermid am 25/05/2019.

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Alana Mcdermid

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English

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