Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BDS2 > FHHD > Flashcards

FHHD Flashcards

(113 cards)

Start Studying
1
Q

What is meant by:

1) ACUTE Inflammation?
2) CHRONIC Inflammation?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 “Cardinal Signs” (Macroscopic changes) in Acute Inflammation?

A

1) Redness
2) Heat
3) Pain
4) Swelling
5) Loss of Function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are Exogenous (5) and Endogenous (4) causes of Acute inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 5 possible outcomes of Acute Inflammation?

Name in order of best to worst…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 5 main Clinical Features of Acute Inflammation?

A

1) Pyrexia (fever)
2) Drowsiness/Lethargy
3) Leukocytosis (increased WBCs)
4) Decreased Appetite
5) Acute phase proteins (liver’s reaction to inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 5 main MICROscopic changes in Acute Inflammation?
Relate each to MACROscopic changes (those seen from naked eye)

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

In Acute Inflammation, what are the 3 types of migration of WBCs?

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Suppurative Inflammation?

What is formed and what are the possible adverse effects of this?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main cells (5) present in Acute Inflammation?

Which predominates in first 6-24 hours? After this?

A

ACUTE

  • Neutrophils (main in first 6-24 hours)
  • Macrophages/Monocytes (main after 24 hours)
  • Basophils
  • Mast Cells
  • Eosinophils (esp in allergen + helminth infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main cellular differences between Acute and Chronic Inflammation?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 main groups of chemical mediators in Inflammation (based on production)?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What Vessel changes occur in Acute Inflammation?

Where is permeability greatest? What does this lead to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What 2 factors dictate the quality of tissue repair?

Regeneration and Resolution (good) vs. Repair (bad)

A

1) Cell type present
Labile and Stable = Regeneration
Permanent = Repair (incapable of mitosis)

2) Tissue architecture - Basement membrane intact?
Intact = Regeneration
Damaged = Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is angiogenesis? Explain the steps in which it occurs (6)

A

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”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is meant by “Repair”?

What are 6 possible complications?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In what 3 ways do Growth Factors control repair?

What is a disorder in GF production, what does it result in?

A
  • Fibroblast activation and proliferation
  • Angiogenesis (new capillaries)
  • Epithelial cell regeneration

E.g. Acromegaly - too much GF produced by Pituitary gland (enlarged and bulbous features)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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)

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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)

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 2 main outcomes of Chronic Inflammation?

A

1) Repair - Stimulus removal allows lost tissue to be replaced with fibrotic scar (via Granulation tissue)
2) Perforation - Stimulus continues, further spread of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the difference between Regeneration and Repair?

Which is best and why?

A

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…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 5 MICROscopic features of Chronic Inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the 5 main types of Hypersensitivity reactions?

Give main cause of each and example

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 2 main Phagocytes present in Acute Inflammation?
How do they function?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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
26
What 3 tissues are the only ones able to Regenerate all constituents?
1) Liver 2) Bone 3) Bone Marrow
27
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)
28
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
29
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
30
``` 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
31
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
32
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 ```
33
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
34
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
35
Name 4 general characteristics/traits of all Clostridium species...
1) Obligate anaerobes 2) Gram +ive rods 3) (Endo)spore-formers 4) Exotoxin formers
36
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)
37
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)
38
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)
39
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
40
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 ```
41
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
42
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
43
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
44
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
45
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 ```
46
What are 9 Staph. aureus Virulence Factors?
1) Enterotoxin/ Pyrogenic (fever) Exotoxins "Super antigens, readily activate T Cells to liberate large amounts of cytokines" 2) Exfoliatins/ Epidermolytic toxins "Mainly A + B Toxins, causing blistering conditions" 3) Toxic Shock Syndrome Toxin (TSST-1) 4) Haemolysins "4 main types: Alpha/Beta/Delta/Gamma. 90% Staph. aureus is ALPHA" 5) Panton-Valentine Leucocidin "Resistance against WBC phagocytosis, common in MRSA" 6) Hyaluronidase "Spreading factor - breaks down Hyaluronic Acid in tissues" 7) Enzymes "Other enzymes, e.g. Protease, Coagulase, DNAse" 8) Cell Wall Polymers - Peptidoglycan (inhibits inflammatory response) - Lipoteichoic Acid (Interacts w/ TLRs Toll Like Receptors) 9) Cell Surface Proteins - Protein A (reacts w/ Fc region of IgG) - Clumping Factor (binds to fibrinogen) - Fibronectin-binding protein
47
What are the functions of Haemolysins? | What are the 4 main types and which one is mainly present in Staph. aureus?
Cytotoxic: Involved in the lysis of RBCs, Phagocytes and Tissue Cells 4 main types: Alpha - Main one in S. aureus (90% = Alpha) Beta Delta Gamma
48
Name 3 Coagulase Negative Staphylococci. In general, what are 3 features that differentiate them from Coagulase Positive Staphylococci (e.g. S. aureus)? How you could differentiate each of the 3 named Coagulase Negative Staph from eachother?
S. epidermis - Novobiocin sensitive S. haemolyticus - Novobiocin sensitive S. saprophyticus - Novobiocin RESISTANT 1) Coagulase -ive on test (no clumping) 2) Non-pigmented (white) 3) DNAse -ive ``` S. epidermis • Novobiocin sensitive • Mannitol fermentation -ive • Gamma haemolytic (NO haemolysis) • Present on normal microflora - common infection involvement ``` S. haemolyticus • Novobiocin sensitive • Resistant to Teicoplanin S. saprophyticus • Novobiocin RESISTANT • Common cause of UTIs
49
What is the main virulence factor for Coagulase Negative Staphylococci? Therefore what infections are they usually involved in?
Formation of an adherent biofilm to surfaces of implants/prosthetics Therefore, common in infected prosthetics (e.g. Prosthetic valve in endocarditis)
50
What is meant by the following terms: 1) Endemic? 2) Epidemic? 3) Outbreak? 4) Pandemic?
1) Disease always present in population at constant level, though may be cyclic (e.g. seasonal colds) 2) Disease found in higher than normal levels 3) LOCALISED incidence in disease outbreak (e.g. E. coli food poisoning) 4) WIDESPREAD EPidemic, spreading between continents (e.g. Cholera)
51
What are the 2 main types of Infective Endocarditis? How do they differ? (Onset, site, severity of destruction and bacterial cause) Which bacteria most likely to infect prosthetic valves in first few months of fit?
1) ACUTE Rapid onset, severe destruction and often on previously healthy valves Causes: Staph. aureus, Strep. pneumoniae + Enterococci 2) SUB-ACUTE Slow onset, less destruction and often on previously abnormal valves (e.g. prosthetics or rheumatic fever) Causes: Oral Streptococci - S. sanguinis, S. mitis or S. mutans N.B. In first few months of prosthetic fit, valves most likely to be colonised by Staph. aureus or Coagulase -ive staph (e.g. S. epidermis/heamolyticus/saprophyticus)
52
What are the most likely bacterial causes of Infective Endocarditis? What do they all share in common?
All Gram +ive cocci 40-60% = Oral Streptococci (e.g. S. sanguinis, S. mitis or S. mutans) or Enterococci 20-40% = Staphycoccus aureus (or other Coagulase -ive staph)
53
What are 5 (less likely) bacterial causes of Infective Endocarditis? (HACEK or Holy Aga Calls Keendra Evil)
``` Haemophilus Aggregatibacter Cardiobacterium Eikenella Kingella ```
54
What are 5 predisposing factors to Infective Endocarditis?
1) Prosthetic valves 2) Congenital Heart Disease/Defect (E.g. BAV) 3) IV Drug users 4) Rheumatic heart disease (causing damage to valves) 5) Iatrogenic - IV or Cannula use
55
Why is Infective Endocarditis difficult to diagnose? What "Criteria" is used to diagnose? (Hint: Explain Major/Minor and how many needed for diagnosis...)
As non-specific symptoms: Fever, Fatigue + Joint pain (Splinter Haemorrhages = more specific sign) "DUKE'S CRITERIA" (Cross-specialty between clinical and lab evidence) MAJOR: - Echocardiogram +ive for vegetation (restricts BF) - 2 +ive blood cultures for IE - Damage to artificial valve - Valvular regurgitation MINOR: - Predisposition (e.g. prev heart disease or IV drug user) - Fever - Antibody response present - Vascular (arterial embolism or septic pulmonary infarcts) - Immunological (e.g. Glomerulonephritis) DIAGNOSIS = 2 MAJOR or 1 MAJOR + 3 MINOR or 5 MINOR
56
In Infective Endocarditis treatment, IV Antibiotics are often given (with 2+ given at one time in "Synergistic Combination") how do the combinations differ based on it being: 1) ACUTE IE? 2) SUB-ACTUTE IE? 3) IE in MRSA or Px allergic to Penicillin? How are all 3 of these the same?
All 3 are the same as always given with: IV Gentamicin 1mg/kg body weight every 8 hours 1) ACUTE IE Flucloxacillin IV 8-12g in 4-6 doses + Gentamicin 1mg/kg body weight every 8 hours 2) SUB-ACUTE IE Penicillin IV 7.2g in 6 doses OR Amoxicillin IV 2g every 6 hours + Gentamicin 1mg/kg body weight every 8 hours 3) IE in MRSA or Px allergic to Penicillin Vancomycin IV 1g every 12 hours + Rifampicin Orally 300-600mg twice a day + Gentamicin 1mg/kg body weight every 8 hours
57
Outline the 4 main steps in Infective Endocarditis development...
1) Irregular blood flow (esp at valves from high to low pressure) 2) Damage → Clot formation (thrombus) 3) Microorganisms adhere to clot - Vegetation forms 4) Vegetations are viable, easily dislodge to block blood flow or spread infection (septicaemia)
58
What type of Infective Endocarditis are Streptococci species most commonly associated with? What are 5 Streptococcal Virulence Factors?
More commonly associated with SUB-ACUTE IE 1) Adherence to Fibronectin (protein on heart endothelium) 2) Adherence to Platelets (via PAAP - Platelet Aggregation Associated Protein) 3) Adherence to Collagen (via PAAP) 4) Proteinase production (degrades tissue) 5) Extra-cellular polysaccharide production (Sucrose storage)
59
What are 3 Cell Surface Proteins found in Staphylococcus aureus that can act as Virulent Factors?
1) Protein A - Binds to Fc region of IgG 2) Clumping Factor - Binds to Fibrinogen 3) Fibronectin-Binding Protein
60
What are the 4 main areas lung cancer can metastasise to?
Bone Brain Adrenal Glands Liver (Think: Bad Breath Attacks Liver)
61
What are the definitions of the following: 1) Atrophy? 2) Hyperplasia? (Where can u not get this?) 3) Hypertrophy? What are 3 possible complications of 2 + 3?
1) Wasting or decrease in size of tissue/organ 2) Increase in tissue/organ due to increase NUMBER OF CELLS (Cant get this in areas with no cell proliferation/stem cells, e.g. in Brain) 3) Increase in tissue/organ due to INCREASED CELL SIZE (usually due to increased cytoplasm) Complications: Obstruction, Infarction or Over-Secretion of hormones
62
What is the difference between Metaplasia and Dysplasia? Which is reversible/irreversible? Which has the potential to become cancerous (is pre-malignant)
Metaplasia (REVERSIBLE) = A change from one mature cell type to a distinctly different mature cell type (NOT cancerous) E.g. Squamous → Glandular in Barrett's Oesophagus Dysplasia (IRREVERSIBLE) + Abnormal cell development (atypia) that hinders cell maturation Pre-malignant/can be cancerous
63
What is meant by a Neoplasm/Tumour? | What are the main types and how are they generically named?
``` Abnormal tissue growth which exceeds and is uncoordinated with adjacent normal tissue and grows autonomously (growth persists after stimulus removed, vs. non-neoplastic growth which stops when stimuli removed) BENIGN or MALIGNANT Benign - Generally end in "-oma" 4 exceptions: Lymphoma, Myeloma, Melanoma and Mesothelioma Malignant: "-carcinoma" = Epithelial cells "-sarcoma" = CT "-blastoma" = Embryonic cells ```
64
What are "Teratoma's"?
Germ Cell Neoplasms (from testes/ovaries) which differentiate along more than one germ cell line. Can be Benign or Malignant but tend to be MALIGNANT and related to INHERITED CANCER
65
What is meant by: 1) Histogenesis? 2) Differentiation? 3) Anaplasia?
1) Cellular origin of a Neoplasm 2) Degree to which Neoplasm resembles original cell 3) [Regression] Loss of differentiation, so cannot tell cellular origin
66
In what 3 ways can Malignant Neoplasms lead to death?
Haemorrhage Metastasis → Multiple organ failure Immune suppression → Opportunistic infection
67
What are the preferential sites of Metastasis for: 1) Lung Cancer? 2) Bone Cancer?
1) Bone, Brain, Adrenals + Liver | 2) Prostate, Lung, Thyroid, Breast + Kidney
68
What are the 3 main types of Environmental Carcinogens? | Give some examples of each and the types of cancer they're linked with
1) CHEMICAL - Cigarettes (Aromatic Hydrocarbons) → Lung - Asbestos → Lung or Mesothelioma - Azo dyes → Bladder cancer 2) RADIATION - Nuclear → Thyroid, Lymphoma or Leukaemia - UV → Skin (SCC, BCC or Melanoma) 3) VIRAL Hep B → Hepatocellular Carcinoma HPV → Cervical Cancer HIV → Karposi's Sarcoma (via HHV8) EBV/HHV4 → Burkitt's Lymphoma or Nasopharyngeal cancer
69
Explain the phrase: | "All cancers have a genetic basis but only some cancers are inherited"
* All cancers have Somatic mutations * Germ Line mutations (Teratomas) have an increased tendency to be malignant and linked to inherited cancers * GATEKEEPER Tumour Suppresser genes are inactivated or down-regulated in cancer. Their inactivation leads to a 1000x increased cancer risk, with only one further mutation necessary to form a neoplasm * Cancer likelihood increases with age (as mutations become more frequent) therefore resulting cancers may not be inherited, inherited gene mutations do not CAUSE the cancer but increase its likelihood
70
What are 4 cancers with high genetic link (often inherited)? (Give relevant gene mutations)
1) Retinoblastoma (PRB) 2) Breast (BRCA1+2 + TP53) 3) Endocrine 4) Colon (APC + HPPC)
71
What are the following: 1) Proto-oncogenes 2) Oncogenes? 3) VIRAL Oncogenes? 4) Tumour Suppressor Genes?
1) Normal gene (often involved in cell growth) which can form Oncogenes if abnormally switched ON... (e.g. by mutation or chromosome rearrangement) 2) Genes with malignant potential (form Proto-oncogenes abnormally switched on) 3) Genes activated by sequence alteration or over-expression and inactivate Tumour Suppressor Genes... 4) Genes abnormally switched OFF/reduced expression in cancer
72
What are the 2 main types of Tumour Suppressor Genes? How do they differ?
1) GATEKEEPER (e.g. PRB, APC, TP53 ) • Regulate tumour growth by controlling cell cycle or promoting cell death • Inactivation → LARGE increase in cancer risk (x1000) - Only one further mutation needed to form a neoplasm 2) CARETAKER (e.g. BRCA1/2, ATM) • Repair DNA or Protect genome from acquiring or retaining DNA damage • Inactivation → SMALL increase in cancer risk (x5-50)
73
1) How are Viral Oncogenes activated? How is this different to Human Oncogenes? 2) What is the Viral Oncogene MOA? 3) Give an example of Viral Oncogene pathway using HPV → Cervical Cancer
1) Activated by sequence alteration or over-expression (vs. Human Oncogene, activated by mutation or chromosome translocation) 2) Inactivates Tumour Suppressor Genes 3) HPV → Encodes proteins E6 + E7 → Inactivate Tumour Suppressor Genes: RB1 + TP53 → Cervical Cancer
74
Are Caretaker Tumour Suppressor Genes Dominant or Recessive? (Explain with examples)
Can be EITHER! 1) DOMINANT (E.g. BRCA1/2) Only 2 further (somatic gatekeeper) mutations needed to cause cancer 2) RECESSIVE (E.g. ATM) 3 further mutations needed to cause cancer (1 germ line and 2 somatic gatekeeper mutations)
75
In what 2 main ways can (Human) Proto-oncogenes become Oncogenes? (Give examples of both)
1) MUTATION - Mutation in Ras → GTP Constantly bound → Constant cell division 2) CHROMOSOME REARRANGEMENT/TRANSLOCATION - Translocation of enhancer sequence next to MYC gene → over-expression of transcription factors → Burkitt's Lymphoma - Translocation of chromosome 9 and 22 in BCR-ABL gene → continual activation producing tyrosine kinase → CML (Chronic Myeloid Leukaemia)
76
What is the main causative organism of TB in humans? | What are 3 diagnostic features of its presence?
M. tuberculosis 1) Positive ZN (Acid fast) stain - red rods on green background 2) Slow growing: LJ Slope growth at 37ºC 3) Appear: "Rough, Buff (yellow) and Tough"
77
Why does M. tuberculosis not gram stain? What stain can be used alternatively?
Because of the outer waxy lipid layer (Mycolic acid) | ZN (Acid-Fast) Stain used as alternative
78
``` What is a Ziehl-Neelsen stain? How is it carried out (4 steps)? What would you expect to see in: 1) Positive stain? 2) Negative stain? ```
Acid- Fast stain 1) Flood sample slide with Carbol fusion (red stain) 2) Heat to steaming (not boiling) point for 3-4 mins to "cook" stain into cell wall 3) Flood slide with acid-alcohol mix (decolourise) and wash with water 4) Counter stain with 0.5% Malachite Green (for 1 minute)
79
What are the 2 uses of Malachite Green in M. tuberculosis culturing/staining?
1) Used in production of ZN stain (final step) | 2) Present in LJ slope as inhibitory agent against other bacterial growth
80
What are the 2 main phases of TB treatment (how long do they last and what drugs are used)?
``` PHASE 1: INTENSIVE (2 months) "RIPE" Rifampicin Isoniazid Pyrazinamide Ethambutol ``` PHASE 2: CONTINUOUS (4-9 months) Rifampicin + Isoniazid
81
What is the Elek Test? | When is it used and what would be seen in a positive or negative result?
Test to determine Toxic from Non-Toxic Corynebacterium diphtheriae strains. Three main strains = Mitis (least toxic), Intermidius and Gravis (most toxic) 3 strips laid out: 2 = Positive and Negative toxin controls 1 = Test strip (sample you're testing) A 4th strip soaked in anti-toxin is laid across all three. POSITIVE result = Line of precipitation seen (between toxin and anti-toxin) NEGATIVE = No line seen
82
What is the main form of (Primary) Liver cancer? | What are 6 predisposing factors?
Hepatocellular carcinoma 1) Hepititis B or C Virus 2) Alcohol 3) Cirrhosis 4) Age + Gender (young men) 5) Haemochromatosis (excessive Fe absorption) 6) Aflatoxin (nuts that taste "off")
83
What are 4 clinical features of Hepatocellular carcinoma?
1) Hepatomegaly 2) Abdominal pain 3) Weight loss 4) Reduced Liver function: may have jaundice/increased bleeding/bruising tendencies
84
What are the Macro (4 )and Micro (3) -scopic features of Hepatocellular Carcinoma?
MACROSCOPIC • Necrotic yellow/white mass (fixed and hard) This may be uni-focal, multi-focal or diffusely infiltrative • Craggy surface • ill-defined outline • Areas of haemorrhage ``` MICROSCOPIC • May be well-differentiated (to resemble normal liver) or poorly-differentiated (metastasis) • High Nuclear:Cytoplasm ratio • Nuclear Pleomorphism is common • High and abnormal mitotic devision ```
85
What 4 cancers often metastasise to cause Hepatocellular Carcinoma?
1) LUNG 2) Breast 3) Colorectal/Stomach 4) Multiple Myeloma
86
What is Cirrhosis?
The IRREVERSIBLE end-stage of Hepatitis, characterised by Fibrosis scarring and disruption of blood flow (via vascular architecture changes)
87
What is Haematochromatosis? | What can it lead to?
``` Inherited condition of excessive Fe absorption. Can Cause: - Diabetes - Cirrhosis - Bronzed/pigmented skin appearance ```
88
What are the 4 main types of immunity?
Passive Natural - Mother to foetus via IgG Passive Artificial - Pre-formed human or animal antibodies for high risk Px • Human (homogenous) = Protection lasts 3-6 months • Animal (heterogenous) = Protection only lasts few weeks Active Natural - Following clinical infection Active Artificial - Vaccine • Viral toxoid (inactivated) • Inactivated/Killed Virus • Attenuated (reduced virulence) Live Vaccine
89
What are the 3 main forms of vaccines? Give examples of each.
1) Viral toxoid (inactivated) - tetanus + diphtheria 2) Inactivated/Killed Virus - tetanus + diphtheria 3) Attenuated (reduced virulence) Live Vaccine - MMR, yellow fever + TB (Mycobacterium bovis)
90
What is an "Adjuvant"? | Give 3 examples
A substance added to a vaccine to enhance the antibody response (mainly added to toxoids and inactivated viruses) 1) Aluminium Hydroxide 2) Aluminium Phosphate 3) Pertussis/Whooping Cough component of combined DTap (Diphtheria, Tetanus and Whooping Cough)
91
How is a vaccine prepared? | What are the 4 main safety problems if proper quality control is not ensured?
Can be prepared using Yeasts - Removal of unwanted proteins and other reactive materials (keep protective antigens to stimulate immune response) - Conjugate vaccine to proteins to provoke immune response Possible Errors: 1) Contamination in the lab! 2) Inadequate inactivation of virus (virus remains active) 3) Inadequate inactivation of toxoids 4) Attenuated live vaccine becomes increasingly virulent
92
What is the main route of Vaccines? | What are the 2 exceptions to this rule?
ALL are Subcutaneous or Intra-Muscular (best anterolateral portion of thigh) Except... Oral Polio Vaccine (OPV) = Oral (colonises gut and present in faeces) BCG (TB) = Intra-Dermal
93
What is Herd Immunity? | Why can this be achieved in TB and Diphtheria but NOT Tetanus?
The idea that if majority of a community (over 90%) receives active immunity against a disease which is normally transmitted between people, the rest of the community will also benefit. (TB + Diphtheria = Transmitted from person to person but Tetanus is NOT!)
94
What is a vaccine given to children in the first 2-18 months? What does this protect against? What are the 2 main issues with vaccinating a child in the first few months of life?
DTap 6: Diphtheria, Tetanus, Whooping Cough/Pertussis (adjuvant), Polio, Haemophilis Influenzae, Hep B. 1) Undeveloped immune response (limited antibody production) 2) Maternal antibodies (passive natural) still present and may reduce or prevent a response
95
What is the difference between Primary (1st) and Secondary (2nd/Booster) Immune Responses with regards to vaccines?
Primary = Slower, Less Antibodies produced + most antibodies are IgM Secondary (booster jab) = More rapid and increased response, More antibodies produced (higher antibody titre) + most antibodies are IgG
96
Why are Live (attenuated) Vaccines given 3 weeks apart? | What 2 main groups of Px would you avoid giving them in?
To reduced risk of reaction (high antibody reaction produced) 1) Pregnancy (cross placenta and infect foetus) 2) Immunosuppressed
97
What bacteria causes Syphilis? | How does it enter to cause infection?
``` Treponema pallidum (Spirochete) Entry via penetrating intact mucous membrane or area of skin abrasion ```
98
What 4 features will you see in Congenital Syphilis?
HUTCHINTON'S TRIAD 1) Ears - Deafness 2) Teeth - Mulberry molars, Notched or Screw-shaped incisors 3) Eyes - Interstitial keratitis Or, "Saddle nose" deformity
99
What are the 3 main stages of Syphilis? | What features are associated at each stage?
1) PRIMARY - First infiltration of bacteria in area - Painless Chancre on external genitals, appears within 3 weeks and disappears in 6 weeks 2) SECONDARY (2-12 weeks later) - Flu like symptoms - Macular/Papular rash on abdominals and extremeties (hands/feet) - "Condyloma lata" - Wart like lesion on genitals - Snail-track ulcer on buccal mucosa 3) TERTIARY (3-30 years later) - Slow, progressive inflammation (often cardiac or neural) - "Gumma" - soft growths with hard necrotic centres
100
What are the 2 types of Chlamydia (C. trachomatis-veneral) cells? Which is infective?
1) Elementary Bodies (EB) - Live OUTSIDE host cell and are INFECTIVE 2) Reticular Bodies (RB) - Live INSIDE host cell and are not Infective (metabolically active, differentiate to form EBs which are released upon host cell lysis)
101
What are 4 UTI pre-disposing factors? | Which is the most common UTI bacterial cause?
1) Gender (more common in Females) 2) Disruption in urine flow (e.g. Catheter or Pregnancy) 3) Prevention of complete bladder emptying 4) Hygiene: Sexual activity or Faecal spread E. coli most common! (As common in faeces)
102
What is the clinical diagnosis of UTI/ "Bacteruria" (by a lab)?
The presence of OVER 10^5 organisms per ml of mid-stream urine
103
What are 3 clinical features of a Lower UTI? | How will an Upper UTI present compared to this?
1) Dysuria (pain on urinating) 2) Cloudy Urine (bacteria present) 3) Prostatitis Upper UTI will have the above and also Fever as the kidney is often involved (Pyelonephritis) Upper UTIs are later stages of a Lower UTI as infection ascends up the tract
104
What are the 3 main forms of Urine samples? | What type of Agar do we want to colonise on?
1) Mid-Stream Urine sample 2) Catheter Urine sample 3) Supra-Pubic Aspirate (remove with a syringe) SELECTIVE MEDIUMS, either: MacConkeys Agar CLED (Cystine Lactose Electrolyte Deficient) Agar
105
What are the 5 main components of MacConkeys Agar?
1+2) Bile Salts and Crystal Violet (selective agents) 3) Sodium Chloride (maintain osmotic medium) 4) Lactose (carbon source) 5) pH Indicator - Turns PINK when lactose-fermenter present (e.g. E. coli) - Turns YELLOW when not (e.g. Salmonella or Proteus mirabilis)
106
What are the 2 main bacterial causes of UTIs? How would you differentiate between the two? What are 3 VIRAL/FUNGAL causes of UTI (rare)?
1) E. coli (most common) 2) Proteus mirabilis E. coli is a lactose-fermenter (will turn MacConkeys Agar pink) but Proteus mirabilis is NOT (turns agar Yellow) Proteus mirabilis is also very motile (can be visualised under microscope) Viral Causes: - Candida - CMV (HHV5) - Human Polyomavirus (JC & BK)
107
What are the 2 main types of fungi? | How do they differ in appearance and reproduction?
1) MOULDS - Hyphae (branching filaments) which may collect as a "Mycelium" mass + reproduce by spores 2) YEASTS - Unicellular + reproduce by branching
108
What are the 2 diagnostic methods for Actinomyces? | What would you expect to see?
1) Gram Stain - Yellow sulphur granules | 2) Modified ZN stain - Gram +ive "Mycelia" centre surrounded by Gram -ive/weakly acid-fast "CLUB LIKE" structures
109
What type of bacterium is Actinomyces?
Gram +ive branching filamentous rod (Facultative anaerobe) Commensal organism but can cause Actinomycosis
110
What are the 3 main types of fungal infections?
All types of _____ "Mycoses" 1) Superficial (e.g. Candidiasis or Ringworm) 2) Subcutaneous - Slow,localised spread 3) Systemic- Rapid, wide-spread
111
What are the 3 main genera causing Ringworm (Dermatophytosis/Tinea)? Which tests can we use to identify two of these?
``` 1) Trichophyton (T. mentagrophyte - Spiral hyphae) 2) Epidermophytom (E. floccusum - Lactophenol Cotton blue stain) 3) Microsporum ```
112
Name 2 opportunistic fungal pathogens and one straight pathogen
Opportunistic: - Candida - Aspergillus ``` Straight Pathogen (Systemic Mycoses) - Histoplasma capsulatum ```
113
What is Zidovudine used for?
Used to manage HIV (or as prophylaxis) | Reverse Transcriptase inhibitor

BDS2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions