Theme 3: Inflammation, Infection and Immunology: Part 2 Flashcards

1
Q

What is an abscess?

A

A collection of pus; a complication of acute inflammation

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2
Q

What two processes occur when neutrophil polymorphs infiltrate during AI?

A
  1. Margination - blood cells attach to endothelium

2. Diapetesis - cells squeeze through endothelial gap

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3
Q

What is phagocytosis?

A
  • opsonisation of particles by IgG or C3

- engulfing

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4
Q

What can happen if abscesses are left untreated?

A

can cause uncontrolled infection around the body (septicaemia)

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5
Q

How do we manage abscesses?

A
  • aim is to remove all of the infected material
  • “incision and drainage”
  • may pack with antiseptic soaked gauze to help granulate
  • surgical excision
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6
Q

What does granulation tissue contain?

A

capillaries, oedema, white cells and fibroblasts

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7
Q

How do we heal wounds?

A
  • angiogenesis occurs (VEGF is a protein that promotes the growth of new blood vessels)
  • fibroblasts proliferate and secrete ECM and collagen
  • fibroblast contraction shrinks the wound
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8
Q

What is an ulcer?

A
  • It is a local defect of an organ or tissue that is produced by removing of inflammatory necrotic tissue
  • loss of area of epidermis and dermis to produce a defect
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9
Q

What are the causes of ulcers?

A
  1. Vascular
    - venous (70%)
    - arterial (10%)
    - mixed (10%)
  2. Other (10%)
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10
Q

What are some rare causes of leg ulcers?

A
  • peripheral neuropathy
  • malignant
  • inflammatorry e.g pyoderma gangrenosum
  • vascular: vasculitis
  • iatrogenic e.g drugs
  • infection
  • metabolic e.g diabetes
  • traumatic e.g burns
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11
Q

What are the risk factors for venous leg ulcers?

A
  1. Valvular incompetence
  2. Previous damage to venous system e.g DVT, hypertension
  3. Obesity, immobility
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12
Q

What would you be looking for when taking a history of patient with suspected venous leg ulcer?

A
  • varicose veins - inherited
  • history of DVT, PE
  • sitting or standing for long periods
  • high blood pressure
  • multiple pregnancies
  • previous surgeries egg knee replacement
  • obesity
  • increasing age and immobility
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13
Q

What is the most common location of a venous leg ulcer?

A

medial gaiter area in lower leg

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14
Q

which are more painful - venous or arterial leg ulcers?

A

arterial

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15
Q

How do arterial ulcers develop?

A
  • plaque builds up in arteries that carry blood to lower limbs
  • overtime plaque hardens and narrows arteries
  • limits the flow of oxygen-rich blood to legs
  • associated with peripheral vascular disease
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16
Q

Risk factors of arterial ulcers?

A
  • diabetes
  • smoking
  • high BP
  • high blood lipids
  • history of ischaemic heart disease, peripheral vascular disease
  • renal failure
  • obesity
  • RA
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17
Q

What would you be looking for when taking a history of patient with suspected arterial leg ulcer?

A
  • intermittent claudication
  • rest pain or paraesthesia
  • pain at ulcer site
  • other symptoms of vascular disease e.g angina
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18
Q

What are you looking for on examination of arterial leg ulcers/

A
  • painful ulcer
  • lower leg/foot
  • loss of hair appendages
  • dry skin
  • cool peripheries
  • pale, cyanotic or pre-gangrenous toes
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19
Q

What are neuropathic ulcers? What are the causes?

A
  • due to distal polyneuropathy
  • under metatarsal heads/heel
  • painless but warm with pulses
  • causes: diabetes, alcohol, B1/b12
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20
Q

What is pyoderma gangrenosum?

A
  • inflammatory ulcer
  • exact cause unknown
  • associated with IBD, RA
  • difficult to treat e.g prednisolone
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21
Q

What is healing by first intention?

A
  • restoration of continuity occurs directly by fibrous adhesion, without formation of granulation tissue
  • results in thin scar - no tissue loss
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22
Q

What is healing by second intention?

A
  • wounds with tissue loss or with margins not apposed
  • granulation islands (red)
  • re-epithelialisation - epidermis grows back
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23
Q

How would an ulcer defect heal? (5 steps)

A
  1. Phagocytosis to remove cell debris
  2. Granulation tissue laid
  3. Organisation
  4. Early fibrous scar - epidermis starts to grow back
  5. Scar contraction
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24
Q

Which proteins mediate healing and repair?

A

various cytokines e.g PDGF, EGF etc

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25
Q

How do you treat venous ulcers?

A
  • they require compression e.g using compression stockings/bandages provide up to 40mmHg pressure
  • bandages used if exudative wounds to hold moisture in
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26
Q

What is ankle brachial pressure index?

A

ratio of the blood pressure at the ankle to the blood pressure in the upper arm
-assesses suitability to apply compression

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27
Q

What is pentoxifylline?

A
  • licensed drug for venous leg ulcers and PAD

- can cause hypotension

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28
Q

What is analgesia?

A

inability to feel pain

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29
Q

in 1900, what were the two leading causes of deaths?

A
  1. influenza and pneumonia

2. tuberculosis

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30
Q

What are the 3 leading causes of death today?

A
  1. heart disease
  2. cancer
  3. stroke
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31
Q

What is the scientific classification of living organisms?

did king Phillip come over for good spaghetti

A
Domain
Kingdom
Phylum
Class 
Order
Family
Genus 
Species
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32
Q

Which gene is used for comparison and identification of bacterial species?

A

16S ribosomal RNA - because its in all bacteria and its highly conserved - there’s only small bits of variation

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33
Q

Which two features on bacteria are only found in gram-negative bacteria?

A
  • fimbriae

- sex pilus

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34
Q

What is the function of the flagella and what are the 4 different types?

A

-responsible for locomotion (motility)
Number and location can vary:
-Monotrichous (one flagella)
-Lophotrichous (multiple on one pole)
-Amphitrichous (one coming from each pole)
-Peritrichous (many all over the bacterial surface)

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35
Q

What are pill / fimbriae?

A

Fimbriae are bristle like short fibres occurs on the surface of bacteria.
Pili are long hair like tubular microfibres like structures present on the surface of bacteria. Fimbriae are present on both Gram positive and Gram negative bacteria. Pili are present only on some Gram negative bacteria.

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36
Q

What is the function of pills/fimbriae?

A
  • aid adhesion to host cells and colonisation -allow bacteria to stick to things which is important during infection
  • can adhere to a specific substrate on cell surface
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37
Q

What is the capsule on bacteria?

A

polysaccharide material protecting bacteria from:

  • phagocytosis/immune attack
  • dessication (drying up)
  • antibiotics
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38
Q

what is the difference between a capsule and a slime layer?

A

capsule - tightly adhered to cell

slime layer - loose adherence to cell

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39
Q

What are endospores?

A

metabolically inert forms of bacteria resistant to many forms of environmental stress e.g temperature
example: genus bacillus

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40
Q

What are bacterial cell walls made of?

A

peptidoglycan

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41
Q

What are the 4 types of cell walls of bacteria?

A
  1. gram positive e.g streptococcus, bacillus, clostridium
  2. gram negative e.g E.coli
  3. mycobacterial
  4. no peptidoglycan e.g chlamydia
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42
Q

Why are bacterial cell walls divided into 2 main classes?

A

It is based on their ability to retain a crystal violet-iodine dye complex after acetone/ alcohol treatment

43
Q

What colour does gram positive bacteria appear after acetone treatment?

A

blue/ purple

44
Q

What colour does gram negative bacteria appear after acetone treatment?

A

red/pink

45
Q

What does it mean if the complex turns colourless?

A

stains unable to penetrate mycelia acid layer e.g mycobacteria

46
Q

How do you perform a gram stain?

A
  1. Flood slide with bacteria with crystal violet
  2. All cells take up dye
  3. Flood with Lugol’s iodine (turns dark red)
  4. All cells appear blue-black
  5. decolourise with acetone
  6. counterstain with red dye
  7. gram positive - blue/purple
  8. gram negative - red
47
Q

What are the 6 shapes of bacteria?

A
  1. coccus (spherical)
  2. rod
  3. spirillum (squiggle)
  4. spirochete
  5. budding and appendaged
  6. filamentous
48
Q

Binary fission and asexual reproduction are examples of which gene transfer?

A

vertical gene transfer

49
Q

Conjugation, transformation, transduction are examples of which gene transfer?

A

horizontal gene transfer - acquisition of DNA

50
Q

How do viruses work?

A

transduction

51
Q

What is the cell wall of fungi made of?

A

chitin

52
Q

what causes thrush

A

candida - yeast

53
Q

How do yeast cells replicate?

A

by budding

can be sexual or asexual

54
Q

What are moulds and what do they cause?

A
  • filamentous fungi
  • commonly cause superficial infections e.g ringworm, athletes foot
  • uncommonly cause severe infections e.g aspergillus
55
Q

What are three types of parasites that can cause disease in humans?

A
  1. protozoa
  2. helminths
  3. ectoparasites
56
Q

What is the structure of a virus?

A
  • nucleic acid core wrapped in protein coat
  • some also have lipid envelope
  • nucleic acid core: can be DNA or RNA
  • retroviruses: RNA> cDNA, reverse transcription
57
Q

Explain the life cycle of a virus (6 steps)

A
  1. Attachment to host cell via specific receptors
  2. Penetration via endocytosis or membrane fusion / binds and engulfs
  3. Uncoating - viral contents released
  4. Viral proteins produced e.g polymerase allows replication, capsid, surface proteins
  5. Assembly - new phage particles assembled
  6. Release via budding, or cell lysis
58
Q

What are prions?

A
  • misfolded protein
  • unlike viruses, no genetic material
  • can be inherited, spread via contaminated material or occur spontaneously
  • aggregate and cause folding of proteins
59
Q

What are some diseases caused by prions?

A
  • creutzfeldt-jakob disease
  • scrapie
  • kuru
60
Q

What is microbiota?

A

all the organisms in a given community

61
Q

What is microbiome?

A

all the genes present within the microbiota

62
Q

What is symbiosis?

A

two or more organisms co-exist in a close physical association

63
Q

What are the 4 types of symbiosis?

A
  1. Mutualism - both organisms benefit from symbiosis
  2. Neutralism - neither organism derives benefit or harm
  3. Commensalism - one organism benefits, the other derives neither benefit nor harm
  4. Parasitism - one organism (parasite) benefits at the expense of the other (host)
64
Q

What are 5 non-sterile sites in the body and what does this mean?

A

Non-sterile sites: conductiva, skin, nasopharynx, vagina, GI tract

  • have normal flora
  • exposed to the environment
65
Q

What might the impact of non-sterile sites be on clinical samples from sterile sites?

A

e. g taking a sputum sample
- obtained by expectoration of lower airway secretions (sterile site) through the upper airway (non-sterile site) - risk of contamination
- same with urine samples and blood cultures

66
Q

What are sterile sites and how is sterility maintained?

A

-no normal flora present
sterility maintained by:
-surface cleaning e.g cilia in lower respiratory tract
-barriers adjacent to non-sterile sites
-physical separation from non-sterile sites e.g closed cavities

67
Q

What is tissue tropism?

A

propensity for a particular organism to grow in a particular habitat

68
Q

What are physical variables that affect growing conditions?

A
  • moisture
  • temp
  • pH
  • O2 availability
  • nature of surface
69
Q

What is the gingival crevice and how is it adapted to its environment?

A
  • in between tooth and gum
  • constant temp
  • most
  • anaerobic environment
  • bathed in nutrients
  • mucosal surface components
  • few physical challenges (toothbrush)
70
Q

Which flora occupy the vagina pre-puberty and post puberty?

A

Pre-puberty: skin flora, lower GI flora (mainly E.coli)

Post puberty: glycogen produced due to circulating oestrogen, skin flora, lactobacillus spp

71
Q

Why does the GI tract have low numbers of bacterial growth?

A

low gastric pH inhibits bacterial growth

-mainly aerobic bacteria

72
Q

What are the benefits of normal flora?

A
  • synthesize vitamins that are absorbed as nutrients by the host (e.g. K & B12)
  • prevent colonization by pathogens by competing for attachment & nutrients
  • induction of cross-reactive antibodies (may have protective effect)
  • oral microbiota (nitric oxide production is essential for vascular health)
73
Q

What is clostridium difficile infection?

A
  • hospital acquired infection
  • main risk factor: antibiotic treatment
  • perturbation of normal colonic microflora allows C.difficile overgrowth
  • leads to toxic production
  • diarrhoea and pseudomembranous colitis
74
Q

What is a faecal transplant and when is it used?

A
  • use of bowel-derived matter for disease treatment goes back 2500 years
  • recently made a comeback to treat recurrent C.difficile infection
75
Q

Which conditions have shown to have diminished bacterial diversity of the gut microbiota?

A
  • obesity

- chrons disease

76
Q

What other conditions has faecal transplants been used as treatment and shown success?

A
  • multiple sclerosis
  • chronic fatigue syndrome
  • ulcerative colitis
  • IBS
  • diabetes mellitus
77
Q

How can normal flora become pathogenic?

A
  1. Overgrowth
    - excessive growth at normal site
  2. Translocation
    - presence at the wrong site
    - spread from one surface to another
    - inoculation into a normally sterile site
  3. Cross-infection
78
Q

Which clinical conditions can be caused by normal flora?

A
  • abscesses
  • pneumonia
  • gastroenteritis, peritonitis
  • urogenital infections
  • endocarditis
  • dental caries
79
Q

What is normal flora?

A

Normal flora are microorganisms that live on another living organism without causing disease

80
Q

What is pathogenicity ad what are the requirements?

A
the capacity of a micro-organism to cause disease (used interchangeably with virulence)
Requirements:
-transmissibility
-establishment in a host
-harmful effect
-persistence
81
Q

What is infectivity?

A

The ability of a micro-organism to become established on/in a host. Mediated by: microbial ligand, host cell surface receptor

82
Q

What is a virulence factor? give examples

A

components of a microorganism which aid its ability to cause infection (infectivity and virulence)
examples:
-facilitation of adhesion
-toxic effect
-interference with host defence mechanisms

83
Q

What is the cycle of infection? 6 steps

A
  1. encounter
  2. entry
  3. spread
  4. evade defences
  5. multiply and damage
  6. disperse (cough, sneeze, singing, talking etc)
84
Q

How can we interrupt the cycle of infection?

A
  • hygiene measures
  • reducing interactions (social distancing)
  • preventing aerosols
  • treatment
  • vaccine
85
Q

What is the incubation period?

A

period between infection within the organism and manifestation of clinical features

86
Q

What is the period of infectivity?

A

Period during which a transmissible organism may be transmitted to another person

87
Q

What are the two sources that infections can arise from?

A
  1. Endogenous sources
    - micro organisms from the host getting into the wrong place
  2. exogenous sources
    - organisms originating from the external environment/ infected individuals
88
Q

Which condition causes fluid to collect in the alveoli of the lungs?

A

bacterial pneumonia

89
Q

What is Gonorrhoea? (cause and symptoms)

A
  • sexually transmitted infection
  • caused by neisseria gonorrhoea
  • symptoms: discharge of pus from urethra, burning sensation, sterility
90
Q

How do you encounter bacterial pneumonia?

A
  • inhalation of air-borne droplets containing pathogen
  • contact with mouth of infected individual
  • contaminated blood
91
Q

How do you encounter gonorrhoea?

A
  • sexual contact with infected individual
  • contact with urethral exudate
  • vertical transmission (mother to child during birth)
92
Q

What are adhesins?

A

proteins that cause adhesions

93
Q

What does pneumococcal surface protein A do?

A

prevents complement-mediated killing

94
Q

What is IgA protease and what does it do?

A
  • an endopeptidase produced by S.pneumoniae and N.gonorrhoea
  • degrades IgA
  • found in mucosal secretions of respiratory tract and urogenital tract
  • binds to pathogens and prevent them adhering to host tissues
95
Q

What are the 4 examples of pathogens ?

A
  1. pneumolysin - secreted by S.pneumoniae, allows pore formation
  2. hyaluronidase
  3. neuraminidase
  4. endotoxin
96
Q

What do hyaluronidase and neuraminidase do?

A

enzymes that target components of interstitial cement in connective tissue (hyaluronic) or epithelial cells (neuraminic)
-if pathogen breaks those down, this provides nutrients, more space for organisms to grow and activates immune system

97
Q

What is endotoxin what does it do?

A
  • a component of the outer membrane in N.gonorrhoeae
  • released on cell death/lysis
  • can cause uncontrolled activation of immune response: inflammation, severe tissue damage, multiple organ failure
  • ‘endotoxic chock’ = sepsis
98
Q

What are the 5 impacts of infection on host organisms?

A
  1. inflammation
  2. abscess formation
  3. excessive host response to endotoxin
  4. toxic effects of exotoxin
  5. granuloma formation
99
Q

What are the effects of inflammation caused by infection?

A
  • response to invasion/ tissue damage
  • activation of complement and clotting systems, fibrinolysis, leukocyte adhesion and production of inflammatory mediators
  • local vasodilation
  • increased vascular permeability
  • phagocytosis
  • effects: erythema, swelling, pain, heat, loss of function
100
Q

What are the clinical features of an abscess?

A
  • the lesion itself (fluid filled fluctuant mass)
  • surrounding inflammation
  • non-specific symptoms of infection e.g anorexia, sweats, malaise, fatigue
101
Q

What is tetanus?

A
  • exotoxin mediated infection (neurotoxin)
  • clostridium tetani
  • infection of dirty wounds
  • toxin production called tetanospasmin
  • inhibits release of inhibitor neurotransmitters in CNS
  • death caused by respiratory paralysis
102
Q

What are other examples of exotoxin-mediated infections?

A
  • cholera
  • diptheria
  • clostridium difficile
  • whooping cough
103
Q

What are some routes of dispersal?

A
  • via respiratory droplets e.g pneumonia
  • sexual contact e.g gonorrhea
  • contamination of food and water e.g diarrhoea
  • blood transfusions
  • sharing needles
104
Q

What does infectious dose mean?

A

number of organisms required to cause infection