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DDT > trigger 4 - sepsis > Flashcards

trigger 4 - sepsis Flashcards

1
Q

which 2 signalling pathways lead to activation of NF-KappaB

A

classical (canonical) pathway

alternative (non-canonical) pathway

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2
Q

IkB is degraded in the proteasome enabling NF-kB transcription factor to…..

A

… translocate to the nucleus and induce gene expression

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3
Q

canonical signalling pathway

A

ligand binds to cell surface receptor (e.g. TLR)
recruitment of adaptors (e.g. TRAF) to cytoplasmic domain of receptor
adaptors recruit IKK complex
phosphorylation and degradation of IkB inhibitor

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4
Q

when does non-canonical signalling pathway occur

A

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

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5
Q

process of non-canonical signalling pathway

A

ligand-induced activation
NF-kB inducing kinase (NIK) phosphorylates and activates IKKa complex
IKKa complex phosphorylates p100
p52/RelB heterodimer processed and liberated

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6
Q

IKK complex

A

core element of NF-kB cascade

made of two kinases and a regulatory subunit

NEMO
IKKa
IKKB

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7
Q

cytokines

A

regulatory molecules that coordinate immune responses

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8
Q

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
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9
Q

binding sites for STAT proteins

A

phosphotyrosine residues on the receptor proteins

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10
Q

JAK

A

JAnus Kinase

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11
Q

STAT

A

Signal Transducer and Activator of Transcription

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12
Q

STAT proteins are latent transcription factors

A

they are always present in the cytoplasm waiting to be activated by JAK

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13
Q

STAT dimer is an active transcription factor

A

travels to nucleus and binds to specific sequences in the DNA

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14
Q

JAK inhibitors

A

drugs that inhibit the kinase activity of JAK

small molecule drugs

e.g. Ruxoltinib and Tofacitinib

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15
Q

what processes does JAK activation stimulate

A

cell proliferation
cell differentiation
cell migration
apoptosis

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16
Q

characteristics of cardiac muscle contractions

A

rapid

short duration

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17
Q

calcium-calmodulin complex

A

activates myosin light chain kinase (MLCK)

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18
Q

MLCK

A

phosphorylates myosin light chains in the presence of ATP

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19
Q

myosin light chains

A

20-kD regulatory subunits found on the myosin heads

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20
Q

MLC phosphorylation

A

leads to cross-bridge formation between the myosin heads and the actin filaments
therefore smooth muscle contraction

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21
Q

reduced phosphorylation of MLC

A

VSM relaxation

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22
Q

cause of reduced MLC phosphorylation

A
  1. reduced release of Calcium by the SR or reduced calcium entry into the cell
  2. inhibition of MLCK by increased cellular concentration of cAMP
  3. phosphatase-activated MLC dephosphorylation
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23
Q

what regulates the degree of MLC phosphorylation

A

G-protein-couple signal transduction pathways

nitric oxide activation of guanylyl cyclase and cGMP formation

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24
Q

the SR re-sequesters calcium

A

using ATP-dependant calcium pump

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25
Q

why is CSF testing used

A

to diagnose a disease affecting the CNS

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26
Q

how is a CSF sample collected

A

lumbar puncture or spinal tap

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27
Q

where is CSF formed

A

choroid plexus

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28
Q

MenB vaccine

A

routinely administered to babies

protects against Meningococcal group B bacteria

infections can cause meningitis and septicaemia

vaccine used is Bexsero

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29
Q

microorganisms causing meningitis and septicaemia

A 
meningococcal
pneumococcal
haemophilus influenzae type B (Hib)
group A/B streptococcal
E. COli
listeria
salmonella
tuberculosis
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30
Q

what ligand causes JAK/STAT signallign

A

cytokines e.g. IFN-y, IFN-a

growth hormone

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31
Q

important of commensal microorganisms

A

out-compete pathogenic bactera
provide vitamins
colonisation resistnace

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32
Q

effects of antibiotics on commensal bacteris

A

reduce their diversty

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33
Q

commensal microorganisms as cause of diesease

A

enogenous infection
switch role and cause disease in weak immune system
produce metabolites used by pathogens

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34
Q

overall effect of meningitis

A

inflammation of lungs and subarachinoid space and psinal cord

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35
Q

types of meningitis

A

bacterial - most severe
viral
non-infectious
recurrent/chronic

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36
Q

symptoms of meningitis

A

headache
fever
rash

sepsis
seizures

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37
Q

diagnosis of meningitis

A

CSF analysis - lumbar puncture
- looking for increased proteins, neutrophils and leukocytes

CT scan/MRI

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38
Q

treatment for viral meningitis

A

none

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39
Q

treatment for bacterial meningtisis

A

vaccines

treatment of assocaited disorders

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40
Q

abnormal permeabiltiy of BBB

A

bacteria infect meninges

systemic inflammation

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41
Q

mechanism of meningitis

A

bacteria colonise and penetrate mucosal membranes
invade CNS and multiply in subarachnoid space
release pro-inflammatory cytokines
swelling and increase in intracranial pressure
oedema

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42
Q

dendritic cell function

A

recognises and endocytoses PAMPs
antigen-presenting cell vis MHC
allows differenatiation o Th cells via cytokine release
links innate and adaptive immune system

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43
Q

dendritic cell structure

A

membrane folds allow maximum interaction with other immune cells

44
Q

co-stimulation of T cells

A

required for full t cell activation
co-stimulatory molecules expressed by both T cell and APC
e..g CD28 binds to CD80

45
Q

strucutre of eosinophils

A

bi-lobed nucleus

small, pink cytoplasmic granules

46
Q

function of eosinophils

A

mechanisms associated with allergies and asthma

circulate in blood and migrate to inflammatory tissues

47
Q

what do eosinophils produce

A

toxic cationtic proteins by degranulation
ROS
enzymes
cytokines

48
Q

when/where do eosinophils develo

A

during haematopoiesis in bone marrow

migrate to blood

49
Q

mechanism of eosinophils

A

chemotaxis
target recognition via Fc receptors
phagocytosis
release destructive enzyme and granules

50
Q

what do neutrophils respond to

A

cytokines

released by mast cells and macrophages

51
Q

3 ways neutrophils kill invading microorganisms

A

phagocytosis
production of ROS
Relase of cytotoxic granules

52
Q

how does neutrophil recruitment increase inflammation

A

they release cytokines and chemokines

e.g. IL-8

53
Q

respiratory burst

A

rapid release of ROS from neutrophils

54
Q

killing mechanisms of NK cells

A

release of granules containing perforin granzyme
fas/fas ligand - death signal - induces apoptosis
TRAIL - TNF-related apoptosis inducing ligand
ADCC - antibody dependent cell-mediated cytotoxicity
release of cytokiens

55
Q

missing self hypothesis

A

NK cells recognise cells that have dont have MHC

caspase killing pathway activated on infected cell

56
Q

what do NK cells respond to

A

recognise and respond to MHC I on infected cells

57
Q

what do monocytes differentiate into

A

macrophages or myeloid lineage dendritic cells

58
Q

what are alarmins

A

endogenous molecules released during infection
often debris from dying cells
e.g. DAMPs

59
Q

what are DAMPs

A

danger/damage associated molecular patterns

60
Q

what recognises alarmins

A

PRRs on innate immune cells

61
Q

release of alarmins from dendritic cells

A

active release

62
Q

effect of alarmins on innate immune cell

A

causes release of pro-inflammatory cytokines

e.g. IFN-y, IL-6, TNF-a

63
Q

uses of alarmins in diagnossis

A

biomarkers of inflammation

64
Q

examples of alarmins

A

heat shock proteins
fibrinogen
own DNA
hyaluronic acid

65
Q

6 types of vaccine

A 
live attenuated
toxoid
subunit
naked dna 
inactivated
conjugated
66
Q

live attenuated vaccines

A

weakened version of the microbe
long-term immunity
not good for immunocompromised patients

67
Q

toxoid vaccines

A

iactivated bacterial toxins
no risk of infection
boosters required

68
Q

subunit vaccines

A

fragments e.g. antigens of pathogen
reduced side effects
boosters required
takes time to identify specific antigen

69
Q

naked dna vaccine

A

pure dna injected into patient
body makes proteins after injection
doesnt work well in humans

70
Q

inactivated

A

pathogens grown in culture then killed by heating or exposure to chemicals
e..g formaldehyde
requires multiple doses

71
Q

conjugated vaccines

A

the outer polysaccharide coat of bacterium
effective aganist coated antigens
no risk of infection
expensive to produce

72
Q

challenges to vaccine production

A

antigenic variation
inadequate access - some countries are poor
high costs of vaccine development
risk safety - working with pathogens

73
Q

antibiotic definition

A

chemical compound that targets essential growth processes against bacteria

74
Q

when is a broad spectrum antibiotic useful

A

if you dont know the disease causing bacteria

works against many bacteria

75
Q

when is a narrow spectrum antibiotic useful

A

works well against specific bacteria

76
Q

effects of bacteriostatic antibotics

A

total cell count plateaus
no cell growth
no cell death

77
Q

bacteriocidal effecs

A

cell death
no cell lysis
total cell count remains the same
viable cell count decreases

78
Q

bacteriolytic

A

cell death and cell lysis

total cell count plummits

79
Q

types of antibiotic

A 
b-lactam
tetracyclin
sulfonamide
quinolone
macrolide
aminoglycoside
80
Q

immediate treatment of sepsis/septic shock

A

antibiotics given intravenously

81
Q

role of NF-kappaB

A

transcription factor that acts during infection to produce different cytokines
cytokines inititate inflammation and recruit immune cells

82
Q

NF-kappaB held inactive by

A

IkB in cytoplasm

83
Q

effect of intracellular ROS on NF-kappaB

A

causes upregulation of NF-kappaB and IKK

84
Q

what are pro-inflammatory cytokines

A

signalling molecules released from immune cells during infection
secreted in response to PAMPs binding to PRRS

85
Q

function of pr-inflammatory cytokines

A

activate T cells
antibody production
make diseases worse - inflammation, fever, tissue destruction

86
Q

types of pro-inflammatory cytokines

A

interleukins
interferons
chemokines

87
Q

what secretes IL-1B

A

Monocytes and macrophages in injured epithelial/fibroblasts

88
Q

effects of IL-1B

A

fever
pain
inflammation

89
Q

effects of INF-y

A

results in complement

activates macrophages and phagocytosis

90
Q

what secretes INF-y

A

lymphocytes

91
Q

effects of IL-6

A

makes acute phase proteins from liver

causes fever

92
Q

effects of TNF-a

A

activates NF-kappaB

activates macrophages

93
Q

role of JAK-STAT

A

extracellular to intracellular signalling pathway

leads to production of transcription factors

94
Q

what is a tyrosine kinase

A

enzyme that can transfer a phosphate group from ATP to a protein in a cell

95
Q

mutations in RTKs

A

means they can be activated without a ligand

causes uncontrolled cell growth

96
Q

what allows amplification of signals

A

kinase phosphorylation cascades

e.g. MAPK, PIP3

97
Q

2 biomarkers of inflammation

A

CRP and complement pathway

ESR - erythrocyte sedimentation rate

98
Q

CRP as a marker of inflammation

A

test blood plasma
levels rapidly increase after 2 hours - peak at 48 hours
levels increase following IL-6 secretion
normal crp < 1mg/L

99
Q

what is CRP

A

c-reactive protein
produced by liver
found in blood plasma

100
Q

what is ESR

A

erythrocyte sedimentation rate

how fast RBC fall through column of blood

101
Q

ESR as a biomarker

A 
slow rate of ESR suggests inflammation
clumping seen if increased fibrinogen 
sensitive test
non-specific
levels of fibrinogen may remain high for several days
102
Q

normal ESR

A

men - 3 mm/h

women 7 mm/h

103
Q

what regulates smooth muscle contraction

A

autonomic NS (para and symp)
hormones
stretching

104
Q

how is contraction transmitted from cell to cell in SM

A

via gap junctions

they are low resistance and allow coordinated contraction

105
Q

characteristics of SM contraction

A

Ca2+ binds to calmodulin instead of troponin

MLCK is activated and phosphorylates light chain on myosin head

106
Q

cross-bridge formation

A

myosin light chain is phosphorylated and binds to actin

107
Q

sliding filament theory

A

myosin head (bound to actin) moves forward
new ATP molecules (ahead) binds to myosin head
old cross-bridge detaches

DDT (12 decks)

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