FHHD Flashcards
What is meant by:
1) ACUTE Inflammation?
2) CHRONIC Inflammation?
1) ACUTE = Early response of living tissue to injury, defence mechanism to ideally resolve, heal and repair
2) CHRONIC = Inflammatory response over a prolonged duration, progressing from ACUTE, where there is a persistant causative agent - balance between further tissue damage, eradication of stimulus and healing (scar formation)
What are the 5 “Cardinal Signs” (Macroscopic changes) in Acute Inflammation?
1) Redness
2) Heat
3) Pain
4) Swelling
5) Loss of Function
What are Exogenous (5) and Endogenous (4) causes of Acute inflammation?
EXOGENOUS:
1) Infection - main!
2) Trauma
3) Chemicals
4) Temperature
5) radiation (e.g. UV sun exposure)
ENDOGENOUS:
1) Antigen-Antibody complex
2) Body Chemicals - stomach acid etc
3) Anoxia (lack of O2 - Infarct)
4) Metabolic products - e.g. Urate crystals in Gout formation
What are the 5 possible outcomes of Acute Inflammation?
Name in order of best to worst…
1) Resolution - spontaneous or via treatment
2) Repair - some tissue lost & replaced w/fibrosis scar
3) Chronic Inflammation - involves further tissue loss and repair
4) Suppurative Inflammation - Increased WBC production of pus (liquefaction of tissue) e.g. Abscess
5) Septicaemia - Heightened inflammatory response, infective organism presence in blood stream
What are the 5 main Clinical Features of Acute Inflammation?
1) Pyrexia (fever)
2) Drowsiness/Lethargy
3) Leukocytosis (increased WBCs)
4) Decreased Appetite
5) Acute phase proteins (liver’s reaction to inflammation)
What are the 5 main MICROscopic changes in Acute Inflammation?
Relate each to MACROscopic changes (those seen from naked eye)
1) Increased RBCs - redness
2) Vasodilation: Increased blood flow - heat
3) Oedema - swelling
4) Increased vessel wall permeability - swelling
5) Formation of exudate
6) Migration of WBCs (Margination, Pavementing or Transmigration)
In Acute Inflammation, what are the 3 types of migration of WBCs?
1) MARGINATION Move to vessel wall, away from RBC flow 2) PAVEMENTING Attachment to vessel wall 3) TRANSMIGRATION/DIAPEDESIS WBC leakage through gaps in endothelial cell wall
What is Suppurative Inflammation?
What is formed and what are the possible adverse effects of this?
Type of Purulent inflammation (pus formation).
Pus is formed by WBC enzymes causing liquefaction of necrotic tissue.
Formation of “Abscess” if walled off and surrounded by fibrous rim - reduced blood flow makes it harder to treat w/antibiotics
What are the main cells (5) present in Acute Inflammation?
Which predominates in first 6-24 hours? After this?
ACUTE
- Neutrophils (main in first 6-24 hours)
- Macrophages/Monocytes (main after 24 hours)
- Basophils
- Mast Cells
- Eosinophils (esp in allergen + helminth infection)
What are the main cellular differences between Acute and Chronic Inflammation?
ACUTE = Cells readily available in the bloodstream
(Neutrophils, Macrophages, Basophils, Mast Cells and Eosinophils)
CHRONIC = Above AND cells less readily available
(Lymphocytes: B+T, Plasma Cells, Histiocytes and Fibroblasts)
What are the 3 main groups of chemical mediators in Inflammation (based on production)?
1) Released by damaged tissue (e.g. Bradykinin from Liver)
2) Circulating in plasma
3) Intracellular - preformed (e.g. Histamine, Serotonin,Lysosomal enzymes) or synthesised in response to stimuli (e.g. Prostaglandins, Leukotrienes, Platelet activating factors, Nitrous Oxide, Cytokines)
What Vessel changes occur in Acute Inflammation?
Where is permeability greatest? What does this lead to?
Initial constriction, then dilation of vessels.
- Increased hydrostatic pressure = Opening of capillary blood vessels + net flow out (normally no net flow)
- Permeability greatest in POST-Capillary venules –> Net flow out (previously net flow in)
Increased permeability causes leakage and swelling
What 2 factors dictate the quality of tissue repair?
Regeneration and Resolution (good) vs. Repair (bad)
1) Cell type present
Labile and Stable = Regeneration
Permanent = Repair (incapable of mitosis)
2) Tissue architecture - Basement membrane intact?
Intact = Regeneration
Damaged = Repair
What is angiogenesis? Explain the steps in which it occurs (6)
Angiogenesis = Proliferation of new capillaries in Granulous tissue formation
1) Enzymes (extracellular proteases) degrade basement membrane of parent vessel wall
2) Formation of branch point in vessel wall
3) Endothelial cells migrate to site of damage
4) Endothelial cell proliferate into cords/buds and join to form tubules
5) Maturation and lumen formation (initially leaky)
6) New tubules interconnect to form a network (“Anastomosis”)
What is meant by “Repair”?
What are 6 possible complications?
Repair = Replacement of lost tissue with fibrous scar tissue (occurs if regeneration cannot occur, architecture disrupted or permanent cell presence)
1) Keloids (overgrowth of scar tissue)
2) Exuberant granulation tissue (proud flesh wound)
3) Loss of function
4) Contractures inhibiting movement
5) Adhesion causing obstruction
6) Stretching (e.g. aneurysm dilation)
In what 3 ways do Growth Factors control repair?
What is a disorder in GF production, what does it result in?
- Fibroblast activation and proliferation
- Angiogenesis (new capillaries)
- Epithelial cell regeneration
E.g. Acromegaly - too much GF produced by Pituitary gland (enlarged and bulbous features)
What are the 2 main situations in which Chronic Inflammation can arise?
What are are 5 possible causes?
(N.B. 3 are related to Infection)
1) Acute –> Chronic (initial stimulus persists, may be rapid transition or repeat acute episodes)
2) “De novo” - WITHOUT proceeding Acute
1) Infection: Pathogen resists host defence (e.g. TB)
2) Infection: Pathogen location allows it to persist (e.g. in Abscesses)
3) Infection: Allergen/Hypersensitivity
4) Autoimmune (e.g. Rheumatoid Arthritis/ Coeliac)
5) Unknown/Idiopathic (e.g. Crohns)
What is “Granulation Tissue”?
How does its outcome differ based on whether its involved in Wound or Fracture (bone) Healing?
What cells are present in GT and what type of Inflammation is it mainly prevalent in?
Granulation Tissue = New Connective Tissue formation (“meshwork of immature tissue”)
1) WOUND Healing
Granulation tissue –> Fibrous Scar
2) FRACTURE Healing (bone)
Signals prevent fibrosis scar formation, Granulation tissue cells proliferate to form Chondrocytes (cartilage forming)
Cells: Epitheliod Macrophages, Fibroblasts,, Mofibroblasts (contract) & Lymphocytes
Can be present in Acute or Chronic - more prevalent in Chronic as more tissue loss
How does wound healing differ in a:
1) Primary Intention? (edges of skin CAN be brought together)
2) Secondary Intention (edges of skin CANNOT be brought together)
1) PRIMARY
Epithelial cells proliferate to form granulation tissue BELOW clot
Granulation tissue –> Fibrosis scar
Neat, Linear scar formed in DERMIS (under keratinocytes) - CANNOT be seen on surface
2) SECONDARY
More granulation tissue formation
GT visible on surface (no epithelial covering)
Myofibroblast contraction (close wound and decrease scar size)
Scar may or may not be visible on surface
N.B. BOTH have initial bleeding and associated clot formation (more in Secondary)
What are the 2 main outcomes of Chronic Inflammation?
1) Repair - Stimulus removal allows lost tissue to be replaced with fibrotic scar (via Granulation tissue)
2) Perforation - Stimulus continues, further spread of inflammation
What is the difference between Regeneration and Repair?
Which is best and why?
Regeneration = replacement of injured cells with those of the same type
BEST as allows for “Restitution” - return to normal structure and function
Repair = Replacement of lost tissue with fibrosis scar tissue
N.B. Wound healing is often a combination of Regeneration and Repair…
What are the 5 MICROscopic features of Chronic Inflammation?
1) Areas of necrosis (apoptosis) and possible abscess formation
2) Increased lymphocyte, plasma cell and Macrophages (Histiocytes)
3) Fibroblast presence - Synthesis of ECM and collagen in Granulation tissue
4) Angiogenesis - new blood vessel formation
5) Repair - Fibrosis and Scar tissue formation
What are the 5 main types of Hypersensitivity reactions?
Give main cause of each and example
TYPE I (Immediate)
Cause: IgE antibody release
Example: Asthma or Anaphylaxis (severe)
TYPE II (Cytotoxic)
Cause: IgM + IgG circulating antibody attachment
Example: Goodpastures syndrome
TYPE III (Immune-Complex mediated)
Cause: Antigen-Antibody complex deposition on tissues (normally cleared by phagocytes)
Example: SLE
TYPE IV (Delayed)
Cause: T Cell response
Example: TB, Coeliac or Organ rejection
TYPE V
Cause: Autoantibodies against hormone receptor (act as analogues)
Example: Graves’ Disease
What are the 2 main Phagocytes present in Acute Inflammation?
How do they function?
1) Neutrophils - predominate in first 6-24 hours
2) Macrophages - predominate after 24 hours
PHAGOCYTOSIS
- “Opsonisation” = Antibody binds to specific antigen, flagging for phagocytosis
- Phagocyte engulfs whole complement via formation of pseudopods
- Killing via lysosome in granules of the phagocyte
What are the 3 main cell categories based on ability to undergo mitotic division? (give 3 examples of tissues with each)
Based on this, which cell type is the only one unable to undergo “Regeneration”?
1) LABILE
Cells continually proliferating (mainly stem cells)
E.g. Skin, Bone marrow + Gut mucosa
2) STABLE
Low level of turnover but can undergo mitotic division in injury
E.g. Kidney, Liver + Endocrine Glands
3) PERMANENT
CANNOT undergo mitotic division or organised proliferation
E.g. Neurones + Cardiac/Skeletal/Striated muscle
Therefore, Permanent cells can never undergo Regeneration, only Repair
What 3 tissues are the only ones able to Regenerate all constituents?
1) Liver
2) Bone
3) Bone Marrow
What are the main steps in Fracture (Bone) Healing?
How does this differ to Wound Healing? What type of cells are present - is this Regeneration or Repair?
1) Initial bleeding, Inflammation, Clot and Granular Tissue formation (same in Wound healing)
2) Granular Tissue signaled NOT to undergo fibrosis (normal fibrotic scar formation in wound healing) and INSTEAD, proliferate to form Chondrocytes
3) Chondrocytes lead to Cartilage formation
4) Cartilage bridges gap between fracture ends (“Provisional Callus”)
5) Provisional (Fibrocartilagenous) Callus ossified by Osteoblasts to form Bony Callus
6) Bone remodelling via Osteoblasts/clasts
7) Woven bone –> Lamellar bone
Labile cells - Regeneration
N.B. This is the ONLY situation in which Granular Tissue leads to Regeneration (all other scenarios GT –> Fibrosis scar/Repair)
What is the definition of:
1) Regeneration?
2) Resolution?
3) Restitution?
4) Repair?
1) REGENERATION = Replacement of injured cells with those of the same type (must be Labile or Stable)
2) RESOLUTION = Complete return to normal structure and function after injury
3) RESTITUTION = Return to normality due to REGENERATION + RESOLUTION
4) REPAIR = Replacement of lost tissue with fibrous scar tissue
Does Granulation Tissue lead to Regeneration or Repair?
What is the only exception to this rule?
Leads to Repair via production of fibrosis scar tissue.
Only exception = Fracture healing (bone) where leads to Regeneration as signals prevent fibrosis
What is meant by the following: 1) Facultative anaerobe? 2) Obligate anaerobe? 3) Microaerophiles? 4) Capnophiles? (Give examples for the first 2)
1) FACULTATIVE ANAEROBE
Organisms that can grow in aerobic or anaerobic conditions (E. coli, Staphylococci or Streptococci)
2) OBLIGATE ANAEROBES
Organisms that are unable to grow in the presence of oxygen (require low reduction/oxidation potential)
(Actinomyces, Clostridium, Fusobacterium, Prevotella etc)
3) MICROAEROPHILES
Organisms that require a small amount of oxygen (but less than normal atmospheric 20% v/v levels)
4) CAPNOPHILES
Organisms that require 5-10% CO2 for growth
What is a Capnophile?
Give 2 examples, what dental disease are they both involved in?
Capnophile = Organism that requires 5-10% CO2 for growth
E.g. Capnocytophaga and Aggregatibacter
Both involved in PERIODONTITIS
What bacterial infection causes “Botulism” and how?
Clostridium Botulinum (Gram +ive, spore-forming, onligate anaerobe rod) Forms (neuro)toxins (A-G) which prevent Acetylcholine release from motor nerve terminals. Human Botulism = A, B + E Infant Botulism = A and B only
What 2 ways can Clostridium perfringens be identified over other Clostridium species?
1) Nagler’s Reaction: C. perfringens produces Lecithinase enzyme, which produces opaque area of destruction when added to egg yolk (Lecithin) agar
2) Produces Alpha toxin which is haemolytic and produces double zone of haemolysis on blood agar
What diseases can the following Clostridium species cause:
1) C. botulinum?
2) C. perfringens?
3) C. difficle?
4) C. tetani?
1) Botulism
2) Gas gangrene, Food poisoning or Antibiotic-related diarrhoea
3) Antibiotic-related diarrhoea or pseudomembranous colitis
4) Tetanus
Name 4 general characteristics/traits of all Clostridium species…
1) Obligate anaerobes
2) Gram +ive rods
3) (Endo)spore-formers
4) Exotoxin formers
1) What is a histological defining feature of C. tetani?
2) What 2 exotoxins are produced by C. tetani and how do they function?
1) Rounded terminal spores = “Drum-stick” Appearance
2) Tetanospasmin (prevents inhibitory NT release, e.g. GABA or Glycine)
Tetanolysin (haemolysin)
What is Gas Gangrene?
What are the symptoms?
What are 5 potential causes?
What are the 3 stages of infection
Gas Gangrene = Gas formation in tissues causing necrosis
Symptoms = Fever, Shock, Deliria, Coma or Death
Causes (all Clostridium) :
C. perfringens, C. histolyticm, C. novyi, C. septicum or C. sordelli
3 Stages of Infection:
1) Contamination with the above
2) Clostridial cellulitis
3) Gas Gangrene (myonecrosis)
What are the 4 main methods of culturing (obligate) anaerobic microorganisms?
What is the main gas present?
1) Anaerobic Jars
2) Anaerobic Cabinet
3) Roll Tube Technique/ “Hungate Method”
4) Robertons Cooked Meat (RCM) Medium
Main gas usually Nitrogen (though can be CO2)
What are the 2 main methods of Anaerobic Jar formation for culturing Obligate anaerobes?
1) Vacuum/Replacement
Air removed with vacuum pump and then replaced with air mix (no O2) and palladium catalyst
2) Gas-Generating Sachet
“Anaerogen sachet” added, this absorbs O2 and produces CO2 to replace
What is the difference between:
Sterilisation, Disinfection and Cleaning?
CLEANING = Physical removal of microbes (but not necessarily killing) often used before Disinfection/Sterilisation DISINFECTION = Removal/Inactivation of SOME but not all microbes - used on Low risk objects (don't come into contact w/ Px or intact skin only) STERILISATION = KILLING and removal of ALL microorganisms
What are the 4 main methods of Sterilisation?
Which is used on clinics? Outline this method.
1) Heat (Moist Heat, e.g. Autoclave on clinics, or Dry Heat)
2) Ionising radiation (e.g. Gamma/X-rays in commercial sterilisation)
3) Gas (Ethylene Oxide in commercial sterilisation)
4) Filtration (0.22nm pore size which excludes all bacteria but NOT Virus’)
AUTOCLAVE (Moist Heat) = Steam at high pressures
• 134-137ºC
• 2.25 Bar pressure
• 3 minutes
Why is Staphylococcus aureus known as “transient members of the oral community”?
Instead, where is it most commonly found and therefore how is it most likely spread?
It is not commonly found in the mouth (not part of the normal microflora).
Most commonly found in the nose (“anterior nares”) where they’re often spread by healthy/asymptomatic carriers (“shedders”) via air-borne droplets
What is MRSA?
What 3 resistant features will they likely have?
What drug is used as final resort? In what case would this fail?
MRSA = Multi-Resistant Staphlococcus aureus
1) Beta-Lactamases (or “Penicillinase”)
2) Mutated Penicillin Binding Proteins
3) Panton- Valentine Leucocidin (resistance against phagocytosis)
Last resort drug = Vancomycin (Glycopeptide)
Van +ive coding = Full resistance
GISA (Glycopeptide-Intermediate Staph. aureus) = Thicker cell wall resulting in increased (not full) resistance
Outline 7 common features/characteristics of all Staphylococci species…
1) Gram +ive cocci
2) Grape-like clusters (histology)
3) Facultative anaerobe
4) 0.5-1 μm
5) Non-motile and Non-Spore forming
6) Catalase +ive
7) Urease +ive
How is the Staphlococcus species classified/sub-divided?
By Coagulase... COAGULASE POSITIVE: - S. aureus COAGULASE NEGATIVE - Sub-divided by NOVOBIOCIN (Antibiotic) SENSITIVE OR RESISTANT NOVOBIOCIN SENSITIVE: - S. epidermis - S. haemolyticus - S. lugdenesis NOVOBIOCIN RESISTANT: - S. saprophyticus
