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Disease, Diagnostics and Therapeutics > Sepsis > Flashcards

Sepsis Flashcards

1
Q

What are 2 challenges of vaccine production

A
  • Pathogenic strains can mutate, and become resistant
  • Route of transmission of the disease can be difficult
  • Some diseases only affect humans, so animal models cannot be used
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2
Q

True or false: ROS activate nuclear receptors such as NF-KB, HIP or p53.

A

True

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3
Q

What are antibiotics

A

used to treat bacterial infections, by killing the pathogens, or preventing them from spreading

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4
Q

What are pro-inflammatory cytokines

A

a communication mechanism which cause inflammation.

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5
Q

What are the symptoms of a cytokine storm

A 
	Fever
	Vomiting/Diarrhoea 
	Rash
	Increased body temp	
	Tachycardia
	Hypertension
	Tachypnoea  resp failure
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6
Q

What are the 4 types of cytokine

A
  1. lymphokines
  2. monokines
  3. interleukins
  4. chemokines
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7
Q

What are monokines produced by

A

mononuclear cells

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8
Q

What are defensins

A

Cationic proteins able to form ion pores in membranes

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9
Q

What are MHCs

A

genes encoding cell surface glycoproteins required for antigen presentation to T cells

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10
Q

Give 3 effects of T reg cells

A
  • Release inhibitory cytokines
  • Release anti-inflammatory cytokines
  • Cause cytolysis of effector cells
  • Act in competition with APC cells
  • Cause cytokine deprivation
  • Turn off dendritic cells
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11
Q

How is meningitis diagnosed

A

It is diagnosed via CSF analysis (from a lumbar puncture)-

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12
Q

Describe COX-2 enzymes

A

induced by inflammation. COX2 inhibitors are selective and have less GI effects

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13
Q

PRR activation leads to what

A

proteasome degradation of IkB.

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14
Q

Describe MHC1 complexes

A

Present on nucleated cells

Interact with cytotoxic T cells

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15
Q

Is IL-10 pro or antiinflammatory

A

antiinflammatory

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16
Q

What are typical symptoms of meningitis

A

headache, fever, neck pain and a non-disappearing rash.

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17
Q

Which of the following are Interleukins responsible for:

  • Antiviral
  • Leukocytes
  • Mediate chemotaxis
  • Different effects, depending on cell picked up by
A

-Leukocytes

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18
Q

Which of the following are Chemokines responsible for:

  • Antiviral
  • Leukocytes
  • Mediate chemotaxis
  • Different effects, depending on cell picked up by
A

-Mediate chemotaxis

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19
Q

In missing self-hypothesis, what are two enzymes which destroy the cell

A

perforin and granzymes

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20
Q

What are interleukins produced by

A

a leukocyte

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21
Q

True or False: STAT are always present in the cytoplasm waiting to be activated by JAK

A

True

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22
Q

proteasome degradation of IkB leads to what

A

NF-KB transcription factor translocates to the nucleus and causes gene transcription of key parts of the immune response

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23
Q

what processes does JAK activation stimulate

A

cell proliferation
cell differentiation
cell migration
apoptosis

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24
Q

True or false:

ROS may have regulatory effects on numerous signalling pathways

A

True

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25
Q

Which cytokine causes the activation of CD8 cells

A

IFN-y

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26
Q

Role of eosinophils

A

Granules release enzymes to kill pathogens.

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27
Q

Describe the nitric oxide pathway of bacteria killing

A

o Highly toxic to bacteria and inhibits viral replication

o NO can bind to iron and deprive bacteria of this element

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28
Q

What does bacterial meningitis show in CSF

A
  • Increase in leukocytes
  • Elevated protein
  • Less than 50% blood glucose
  • Gram staining needed
  • PCR if available
  • Bacterial culture needed
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29
Q

Describe MHC2 complexes

A

Present on antigen presenting cells

Interact with T helper cells

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30
Q

Which of the following are Cytokines responsible for:

  • Antiviral
  • Leukocytes
  • Mediate chemotaxis
  • Different effects, depending on cell picked up by
A

-Different effects, depending on cell picked up by

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31
Q

What are alarmins

A

endogenous molecules released after infection or tissue damage (aka DAMPs).

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32
Q

What are lymphokines produces by

A

activated T cells

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33
Q

What are the two layers of gram-negative bacteria

A

peptidoglycan layer

lipopolysaccharide

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34
Q

What are cytokines

A

proteins are secreted into the bloodstream to regulate the immune response

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35
Q

What are commensal microorganisms

A

the beneficial microorganisms present on the body surfaces which are covered by epithelial cells such as the GI and respiratory tract

36
Q

What is CRP

A

C reactive protein. a non-specific serum marker of acute inflammation, appearing hours after damage or infection.

37
Q

Explain the mechanism of JAK/STAT signalling

A
  1. ligand binds (e.g. cytokine)
  2. receptor dimerisation activates JAK phosphorylation of receptor
  3. STAT binds to phosphorylated receptor
  4. JAK phosphorylates STAT
  5. STAT dimer forms
  6. STAT dimer travels to nucleus
  7. STAT dimer binds DNA and changes gene expression
38
Q

Define pleiotropic effect of cytokines

A

One cytokine has many effects on different cells

39
Q

Hypochlorous acid is produced from what?

A

hydrogen peroxide and chlorine

40
Q

What are vaccinations

A

an injection containing a version of the pathogen. They trigger an immune response in the body so that if you encounter the pathogen again, then the secondary immune response is faster and more effective.

41
Q

In bacterial infections, how do dendritic cells activate T helper cells

A

by presenting a peptide part of the pathogen to the T Helper (TLR) on the MHC 2 surface molecule

42
Q

when does non-canonical NFKB signalling pathway occur

A

during the development of lymphoid organs responsible for generating B and T lymphocytes

43
Q

Role of natural killer cells

A

Induce apoptosis in virus. Release perforin, which ruptures the viral membrane

44
Q

What are the 5 types of vaccines

A 
Live attenuated
Dead
Toxoid
Conjugate
DNA
45
Q

True or false: a cytokine storm is a negative feedback loop of cytokine and immune cell signalling.

A

False- positive feedback loop

46
Q

What is the function of chemokines

A

create a chemotactic gradient for immune cells to follow to the required site

47
Q

Which of the following are Interferons responsible for:

  • Antiviral
  • Leukocytes
  • Mediate chemotaxis
  • Different effects, depending on cell picked up by
A

-Antiviral

48
Q

What are the 5 basic mechanisms of antibiotic action

A
  1. Inhibition of Cell Wall Synthesis (most common mechanism)
  2. Inhibition of Protein Synthesis (Translation) (second largest class)
  3. Alteration of Cell Membranes
  4. Inhibition of Nucleic Acid Synthesis
  5. Anti-metabolite Activity
49
Q

What is an cytokine storm

A

a severe immune reaction and can have devastating consequences.

50
Q

What are the receptors which phagocytes possess to bind to antibodies

A

FcR

51
Q

State two roles of commensal microorgansims

A

mucosal immune system
metabolic role
Protective functions
Structural function

52
Q

Why is it bad to miss an antibiotic dose

A

can lead to bacterial resistance, as the weaker pathogens are killed first, and the stronger ones are killed last. If the course is not finished, these stronger ones remain, causing more serious infection

53
Q

Does the activation of T reg cells up or downregulate the immune response

A

Downregulate

54
Q

What is the function of DAMPs/Alarmins

A

They stimulate signalling pathways which initiate innate and adaptive immune responses, triggering inflammation or tissue repair, and directly sense and report damage by signalling to the environment when released from live cells undergoing physiological stress.

55
Q

How can an increase in immune signalling lead to death

A

immune signalling leads to inflammation, which causes the destruction of tissue, and loss of organs resulting in death.

56
Q

Role of neutrophils

A

Locate pathogens through chemotaxis. Granules contain enzymes which kill engulfed pathogens

57
Q

When arachidonic acid is turned into cyclooxygenase, what is this turned into?

A

Endoperoxides- COX1 and COX2

58
Q

What is meningitis

A

An inflammation of the meninges and subarachnoid space

59
Q

When arachidonic acid is turned into lipoxygenase, what is this turned into?

A

Leukotrienes

60
Q

Describe missing self-hypothesis

A

Cells that express self-MHC class I molecules are protected from NK cells, but those that lack this self-marker are eliminated by NK cells.

61
Q

Give two ROS involved in the oxidative burst

A

Nitric oxide
Superoxide
Hydrogen peroxide
Hydroxyl radical

62
Q

What are prostanoids

A

tissue specific isomerases

63
Q

What can a cytokine storm be treated by

A

corticosteroids- which bind to cytoplasmic and nuclear receptors on the cell surface

64
Q

Role of dendritic cells

A

Engulf the pathogen, process antigens, and present them on the CSM using MHC II molecules

65
Q

Phospholipase A2 –> ?

A

Arachidonic Acid

66
Q

What is the respiratory burst

A

After opsonin/ligand binding to cell surface receptors, the active NADPH oxidase is assembled to generate superoxide (O2*) in phagocytes.Superoxide spontaneously dismutates into hydrogen peroxide (H2O2), which may then react with chloride ions to form hypochlorous acid (HOCl), in a reaction catalysed by myeloperoxidase.

67
Q

Give 2 classes of antibiotics

A
  • B-lactam
  • Glycopeptides
  • Sulphonamides
  • quinolones
  • tetracyclin
  • aminoglycosides
  • macrolides
  • amphenicols
68
Q

In viral infections, the virus is released into the tissue. The epithelial cells present a peptide portion of rhe virus on which MHC

A

MHC1

69
Q

What in addition do the cell walls of gram-positive bacteria have

A

peptidoglycan with 2 additional acids: alternating N-acetylglucosamine and N-acetylmuramic acid

70
Q

What does viral meningitis show in CSF

A
  • Lymphocytes increased
  • Elevated protein
  • Usually normal blood glucose
  • PCR if available
  • IgM needed
71
Q

Explain the steps of NF-KB pathway

A
  1. a ligand binds to the receptor on the cell surface membrane causing conformational change
  2. this phosphorylates iKK activating it
  3. IkK phosphorylates iKB
  4. IkB is tagged with ubiquitin and sent to the proteasome to be degraded
  5. ikb dissociates from NF-KB
  6. NF-KB translocates to the nucleus where it starts transcription
  7. when negative feedback occurs, iKBa is transcribed and inhibits NF–KB
72
Q

What are PAMPS

A

exogenous molecules found on pathogens which can be recognised by pattern recognition receptors (PRR)

73
Q

When the effector T cell is activated (bacterial), which cytokine is released

A

IL-2

74
Q

Describe the process of neutrophil attraction to a damaged site

A
  1. Damage occurs, and bacteria enters the tissue
  2. PRR on macrophages binds to the PAMPS on the bacteria and then phagocytosed
  3. Cytokines are released to surrounding tissues
  4. Mast cells are activated and degranulate, which causes blood vessels to become leaky
  5. Neutrophils enter through the gaps (drawn by cytokines) and cause phagocytosis
75
Q

If TNFa pro or antiinflammatory

A

proinflammatory

76
Q

Give three examples of prostanoids

A

prostaglandins
Prostacyclin
Thromboxane

77
Q

Describe COX-1 enzymes

A
  • constitutive. Synthesise prostaglandins and inhibit gastric acid secretion, promoting mucus secretion
78
Q

Role of monocytes/macrophage

A

Phagocytes engulf pathogens and hydrolytic enzymes destroy the pathogen

79
Q

Explain the steps of phagocytosis

A
  • Phagocytes extend their membrane round the microbe.
  • forms a phagocytic vacuole.
  • Microbe then exposed to lysosomal-independent killing mechanisms.
  • The phagosome may also fuse with a lysosome, forming a phagolysosome.
  • The microbe is then exposed to lysosomal-dependent killing mechanisms.
80
Q

What are the binding sites for STAT proteins

A

phosphotyrosine residues on the receptor proteins

81
Q

State 3 pro-inflammatory cytokines

A

IL-1B
IFNY
IL-6
TNFa

82
Q

What types of general effects may cytokines have

A
  • pleiotropic
  • synergistic
  • antagonistic
  • cascade
83
Q

What is the Arachidonic Acid Pathway

A

Inflammation mediated by unsaturated fatty acids- pain fever, vascular permeability, and chemotaxis.

84
Q

What can cause meningitis

A

may result from infections, other disorders, or reactions to drugs

85
Q

In missing self- hypothesis, if cells express MHC 1 molecules, what happens?

A

protected from NK cells, but those that lack this self-marker are eliminated by NK cells

Disease, Diagnostics and Therapeutics (14 decks)

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