Session 3 Lecture Notes Flashcards

1
Q

What is a purpuric non-blanching rash?

A
Purpuric = little purple/red dots on skin - small bleeding of blood vessels near skin surface 
Non-blanching = the spots are fixed / do not go clear when pressed
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2
Q

What is the definition of sepsis?

A

It is a life threatening organ dysfunction due to a disregulated host response to infection

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3
Q

What is septic shock?

A

Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation

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4
Q

What is bacteraemia?

A

Presence of bacteria in the blood

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5
Q

Is sepsis a type of infection?

A

NO!!!!

It is a response to infection

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6
Q

What is the Early warning score? At what score should patients be reviewed for sepsis?

A

EWS = basic observations scored such as respiratory rate, heart rate, temp and blood pressure
Anything over 3 = review for sepsis

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7
Q

What are the Six sepsis bundle?

A
  1. Oxygen
  2. Blood culture
  3. IV antibiotics
  4. Fluid challenge
  5. Lactate
  6. Measure urine output
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8
Q

What should you always do before giving antibiotics?

A

Take a blood culture

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9
Q

What is a good inflammatory marker?

A

C reactive protein

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10
Q

What is the bacterial pathogen that causes meningococcal meningitis?

A

Neisseria meningitidis

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11
Q

How is neisseria meningitidis spread?

A

By direct contact with respiratory secretions

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12
Q

If a bacteria has a lipopolysaccharide complex what does this mean?

A

It is an endotoxin = gram negative bacteria

The endotoxin has the ability to promote an intense inflammatory response

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13
Q

What do the pilli on a bacteria do?

A

Enhance attachment - help the pathogen attach onto host cell

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14
Q

What does the polysaccharide capsule on a bacteria do?

A

Help to protect the pathogen from the body’s defence systems

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15
Q

Name some examples of cytokines

What do cytokines do?

A

Tumour necrosis factor
Interleukin 1
Cytokines stimulate the inflammatory response
They lead to activation of the humeral cascade, activation of thrombin and inhibit fibrinolysis

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16
Q

What does inhibiting fibronolysis do?

A

Prevents fibrin being broken down

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17
Q

What is the major cause of shock and multi organ failure?

A

Microvascular injury

damage to small blood vessels preventing oxygen and nutrients getting to vital organs

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18
Q

What causes progressive necrosis?

A

When blood supply becomes compromised - the blood is reassigned to vital organs and some parts of the body will be compromised eg hands and feet

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19
Q

What are some of the life threatening complications of meningococcal meningitis?

A
  1. Irreversible hypotension
  2. Respiratory failure
  3. Kidney failure
  4. Raised intracranial pressure
  5. Necrosis of hands and feet
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20
Q

How can you confirm diagnosis of meningococcal meningititis?

A
  1. Blood culture
  2. PCR of blood - to look for fragments of pathogen
  3. CSF PCR - as this pathogen
    specifically affects cerebral spinal fluid
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21
Q

What type of bacteria is neisseria meningitidis?

A

Gram negative diplococcus

  • it is an endotoxin
  • has a lipopolysaccharide outer membrane
  • groups of cocci (round shaped)
  • stains pink/red on counter stain
  • polysaccharide capsule
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22
Q

What is the most common strain of neisseria meningidis in the U.K.?

A

Group B

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23
Q

What are the 2 preventions you can take for neisseria meningidis?

A
  1. meningococcal C vaccine

2. antibiotic prophylaxis (preventative treatment given to those close to infected person)

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24
Q

What 2 factors can determine the outcome of the host pathogen relationship?

A
  1. Infectivity (ability to express)

2. Virulence factors (the way the pathogen damages the host)

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25
Q

What is the immune system?

A

Cells and organisms that contribute to immune defences against infectious and non-infectious conditions

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26
Q

What is an infectious disease?

A

When the pathogen succeeds in evading or overwhelming the host’s immune defences

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27
Q

Can you have an adaptive immunity without an innate immunity?

A

NO

The only way the adaptive response will be activated is if dendritic cells do this (if pathogen gets past innate system)

28
Q

Give 3 examples of physical barriers to pathogens

A
  1. Skin
  2. Mucous membranes
  3. Bronchial cilia
29
Q

Give 4 examples of examples physiological barriers

A
  1. Diarrhoea
  2. Vomiting
  3. Coughing
  4. Sneezing
30
Q

What bacteria in the vagina produces lactic

acid to increase acidity and prevent infection?

A

Lactobacillus

31
Q

Give 2 examples of chemical barriers

A
  1. Low pH

2. Antimicrobial molecules eg IgA, lysozymes and mucus

32
Q

Where can an endogenous source of infection come from?

A

From within the body - the normal flora (or microbiota) moving to a location it isn’t normally found

33
Q

Give an example of a normal flora bacteria found on the skin

What infection can it cause?

A

Staphylococcus aureas

It can cause cellulitis

34
Q

Where should the normal flora only ever be found?

A

On the skin or around points of entry (where there is a mucus membrane)
Never in the blood, organs or tissues

35
Q

How can antibiotics lead to thrush?

What is the organism that causes thrush - is it endogenous or exogenous?

A
Antiobiotics can reduce the levels of normal flora 
Candida albicans (a yeast - eukaryotic cell) is able to multiple and causes a yeast infection (thrush)
It is an endogenous source of infection
36
Q

Give 2 examples of bacteria from the normal flora of the respiratory tract that can cause infection

A
  1. Streptococcus pneumoniae

2. Neisseria meningitidis

37
Q

Give examples of 3 common routes the normal flora can use to get into a sterile location (and cause infection)

A
  1. Breaching the skin integrity (eg burns, cut, IV lines)
  2. Fecal-oral route
  3. Fecal-perineal-urethral route (eg UTI)
38
Q

What is the major route in which bacteria from our normal flora gets into the bloodstream?

A

Poor dental hygiene or dental work

39
Q

What should be prescribed to asplenic patients?

A

Antibiotic prophylaxis

40
Q

What is the body’s way of trying to localise/contain an infection?

A

Inflammation

41
Q

Name the 3 main phagocytes

A
  1. Macrophages
  2. Monocytes
  3. Neutrophils
42
Q

Which WBC produces cytokines?

A

Macrophages

43
Q

What WBCs are recruited by chemokines to site of infection?

A

Neutrophils

44
Q

What happens to neutrophils after they destroy bacteria?

A

They die and form pus

45
Q

What is the difference between mast cells and basophils?

A

Mast cells are fixed in the tissue whereas basophils circulate in the bloodstream

46
Q

What is the function of basophils and mast cells?

A

They are early actors of inflammation and important in allergic reactions

47
Q

What is the function of eosinophils?

A

They defend against multi-cellular parasites (i.e. worms or helminths)

48
Q

What is the function of natural killer cells?

A

To kill all abnormal host cells (infected or malignant)

49
Q

What do dendritic cells do?

A

Activate the adaptive immune response

They present pathogens to T cells

50
Q

How do PAMPs help in identifying a pathogen?

A

They are components that may be present on the pathogen that are not present on the host cell
(pathogen associated molecular patterns - such as carbohydrates, lipids or proteins)

51
Q

What are pathogen recognition receptors?

Give an example

A

Example: Toll like receptors

They are receptors on the surface of phagocytes. They recognise the PAMPs on the pathogen - marking it out as a pathogen

52
Q

What is good about toll like receptors?

A

They are present on the cell surface of phagocytes as well as inside the cell
This is key for identifying viruses which have to get inside a host cell to cause an infection

53
Q

Give 2 examples of gram negative bacteria and the pathogen recognition receptor for these (PRR)

A
  1. Lipopolysaccharide (TLR4 PRR)

2. Lipoproteins and lipopeptides (TLR2 PRR)

54
Q

Give 2 examples of gram positive bacteria and the type of pathogen recognition receptors for these

A
  1. Peptidoglycan (TLR2 PRR)

2. Lipoteichoic acids (TLR4 PRR)

55
Q

A phagocyte can recognise all gram negative and positive bacteria using which 2 PRRs? (pathogen recognition receptors)

A
  1. TLR2

2. TLR4

56
Q

What is involved in the opsonisation process?

A

Coating proteins called opsonins bind to the pathogen surface which enables enhanced attachment for phagocytes

57
Q

Give 3 examples of opsonins

A
  1. Complement proteins (such as C3b)
  2. Antibodies (such as IgG)
  3. Acute phase proteins (such as CRP)
58
Q

What are opsonins essential for clearing?

A

Encapsulated bacteria

59
Q

Name 3 types of encapsulated bacteria

A

SHiN

  1. Streptococcus pnuemoniae
  2. Haemophilus influenzae b
  3. Neisseria meningitidis
60
Q

When phagocytosed what does the pathogen become fused with?

A

A lysosome to become a phagolysosome

61
Q

What 2 pathways have we learnt that are activated by the complement proteins?
Which acts earlier and why?

A
  1. Alternative pathway

2. MBL pathway - acts later because the mannose binding lectin has to be produced by the liver in response to infection

62
Q

What complement proteins act as chemotaxins?

What does this mean?

A

C3a and C5a - they attract neutrophils and macrophages

63
Q

What complement proteins act as opsonins?

A

C3b and C4b

64
Q

What complement proteins help in the killing process of bacteria by punching holes in the membrane?

A

C5-C9

65
Q

Give 3 examples of cytokines

A
  1. Tumour necrosis factor a (TNFa)
  2. Interleukin 1 (IL-1)
  3. Interleukin 6 (IL-6)