Session 3- Sepsis, Meningitis and Adaptive Immunity Flashcards
what is sepsis
characterised by a life threatening organ dysfunction due to dysregulated host response to infection
what causes sepsis
vasodilation
capillary leakage
amplification of the immune system
clinical features of infection
rubor calor dolor tumour loss of function
respiratory physiological features of sepsis
raised respiratory rate (tachypnoea). Peri-capillary oedema and reduced pulmonary compliance
cardiac physiological features of sepsis
low BP
tachycardia and end organ damage
CNS physiological features of sepsis
reduced blood perfusion to brain confusion drowsiness slurred speech agitation anxiety reduced level of consciousness
renal physiological features of sepsis
reduced renal output
management of sepsis
BUFALO
3 in 3 out
in: oxygen, antibiotics and fluids if appropriate
out: blood cultures, lactate and Hb, urine output
naiive t cells
havent seen the antigen before
effector cells
have seen the antigen before and respond in particular ways depending on the APC
if its a macrophage then t cells phagocytose the pathogen.
if its a B cell thne t cells respond by stimulating the production of antibodies
where are APCs found
Mucosal membranes skin blood- plasmacytoid cells lymph nodes spleen
what do APCs do
they present pathogen antigenic peptide attached ti MHC.
where are MHC II expressed
dendritic cells
b cells and macrophages
they present microbial peptides from extracellular micobes
where are MHC I expressed
all nucleated cells and present microbial peptides from intracellular microbes.
endogenous pathway
- the virus enters the cytosol
- detected by a proteosome
- broken down the viral peptides
- transported into ER via TAP proteins
- leaves the cytoplasm to present to an a CD8+ T cell
exogenous pathway
- bacteria enters cell via phagocytosis/ micropinocytosis
- broken down in endosomes
- endosomes fusing with large vesicle containing MHC CLASS 2 complex
- presented to CD4+ T cell by APCs only
what are the three main layers - meninges
pia mater- closest to the brain and spinal cord
arachnoid- in the middle
dura mater- outermost layer
what is meningitis
inflammation of the meningeal lining of the brain and spine
what bacteria cause meningitis
Neisseria meningitidis
streptococcus pneumoniae
haemophilus influenzae
viruses that cause meningitis
enterovirus - echoviruses
fungi that cause meningitis
crytococcus neoformans
clinical features of meningitis
general infection features
headache photophobia vomiting neck stiffness on flexion of neck irritable
septic shock
occurs when severe sepsis leads to circulatoty failure and metabolic abnormalities, defined as persisting hypotension requiring active medical treatment and biochemical evidence of disturbed metabolism
causative agents of sepsis
gram-negative infections
investigations of sepsis
obtain samples for microbiology
blood cultures
urine sample
CSF sample
management of sepsis
give high flow oxygen take blood cultures give IV antibiotics Give a fluid challenge measure lactate measure urine output
treatment of sepsis
antimicrobial therapy- rapid,
supportive treatment- treat hypoxia and ensure good tissue oxygenation and intravenous fluids to optimize tissue perfusion. Vasopressors and inotropes may be required in septic shock, mechanical ventilation for severe pneumonia or acute respiratory distress syndrome and renal replacement therapy for acute kidney injury.
the endothelium and coagulation system
Activated endothelium not only allows the adhesion and migration of stimulated immune cells, but becomes porous to large molecules such as proteins,
resulting in the tissue oedema.
Alterations in the coagulation systems include
- increase in procoagulant factors, such as plasminogen activator inhibitor type I and tissue factor
- reduced circulating levels of natural anticoagulants.
Clinically this is seen as clotting in small vessels but often a tendency to bleeding at other sites.
what is the difference between meningitis and septicaemia
meningitis- bacteria in the cerebrospinal fluid that surrounds the brain and spine
septicaemia- bacteria in the blood
what is DIC
Disseminated intravascular coagulation is a syndrome of widespread
intravascular activation of coagulation.
what is petechiae
A petechial rash is
commonly associated with a low platelet count and is a tiny bleed into the skin.
Petechiae of meningococcemia are usually larger and bluer than pinpoint petechiae
caused by thrombocytopenia – reflecting the complex pathophysiology of DIC and
meningococcal sepsis
tumbler test
the rash doesnt blanch when pressure is applied
eccymoses
The petechial lesions can coalesce and form larger lesions that
appear ecchymotic. Ecchymoses (diameter >10 mm) are mainly noted in patients
with severe DIC. These lesions are secondary to subcutaneous hemorrhage.
management of Neisseria meningitdis septicaemia
Early recognition
Early administration of antibiotics. The recommendation if Neisseria
meningitidis is suspected is to give intravenous CEFTRIAXONE
Urgent investigation
Supportive care, often in an intensive care unit to manage organ
dysfunction and DIC.
Notify Public Health
Prevention
mechanism of DIC
The main mechanisms of DIC are inflammatory cytokine-initiated activation of tissue factor-dependent coagulation and insufficient control of anticoagulation pathways. At a simplistic level the coagulation process goes out of control. Lots of small clots form. These use up many of the
anticoagulation factors. The consequence is that there is bleeding occurring at the same time as the small clots are being formed.
what is neissera menigitidis
gram negative cocci
common causes of pneumonia
streptococcus pneumoniae
haemophilus influenzae
staphylococcus aureus
lobar pneumonia
pulmonary consolidation demarcated by border of lung segment or lobe
bronchopneumonia
patchy consolidation around the larger airways
interstitial pneumonia
fine areas of shadowing in the lung fields and there is usually no sputum production at presentation
clinical features of pneumonia
fever malaise tachypnea tahcycardia shock if severe
