Session 3- Sepsis, Meningitis and Adaptive Immunity

Question 1

what is sepsis

Answer 1

characterised by a life threatening organ dysfunction due to dysregulated host response to infection

Question 2

what causes sepsis

Answer 2

vasodilation
capillary leakage
amplification of the immune system

Question 3

clinical features of infection

Answer 3

rubor 
calor
dolor
tumour 
loss of function

Question 4

respiratory physiological features of sepsis

Answer 4

raised respiratory rate (tachypnoea). Peri-capillary oedema and reduced pulmonary compliance

Question 5

cardiac physiological features of sepsis

Answer 5

low BP

tachycardia and end organ damage

Question 6

CNS physiological features of sepsis

Answer 6

reduced blood perfusion to brain
confusion
drowsiness
slurred speech
agitation
anxiety
reduced level of consciousness

Question 7

renal physiological features of sepsis

Answer 7

reduced renal output

Question 8

management of sepsis

Answer 8

BUFALO
3 in 3 out
in: oxygen, antibiotics and fluids if appropriate

out: blood cultures, lactate and Hb, urine output

Question 9

naiive t cells

Answer 9

havent seen the antigen before

Question 10

effector cells

Answer 10

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

Question 11

where are APCs found

Answer 11

Mucosal membranes
skin
blood- plasmacytoid cells
lymph nodes
spleen

Question 12

what do APCs do

Answer 12

they present pathogen antigenic peptide attached ti MHC.

Question 13

where are MHC II expressed

Answer 13

dendritic cells
b cells and macrophages

they present microbial peptides from extracellular micobes

Question 14

where are MHC I expressed

Answer 14

all nucleated cells and present microbial peptides from intracellular microbes.

Question 15

endogenous pathway

Answer 15

• 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

Question 16

exogenous pathway

Answer 16

• 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

Question 17

what are the three main layers - meninges

Answer 17

pia mater- closest to the brain and spinal cord

arachnoid- in the middle

dura mater- outermost layer

Question 18

what is meningitis

Answer 18

inflammation of the meningeal lining of the brain and spine

Question 19

what bacteria cause meningitis

Answer 19

Neisseria meningitidis
streptococcus pneumoniae
haemophilus influenzae

Question 20

viruses that cause meningitis

Answer 20

enterovirus - echoviruses

Question 21

fungi that cause meningitis

Answer 21

crytococcus neoformans

Question 22

clinical features of meningitis

Answer 22

general infection features

headache
photophobia
vomiting 
neck stiffness on flexion of neck
irritable

Question 23

septic shock

Answer 23

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

Question 24

causative agents of sepsis

Answer 24

gram-negative infections

Question 25

investigations of sepsis

Answer 25

obtain samples for microbiology blood cultures urine sample CSF sample

Question 26

management of sepsis

Answer 26

``` give high flow oxygen take blood cultures give IV antibiotics Give a fluid challenge measure lactate measure urine output ```

Question 27

treatment of sepsis

Answer 27

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.

Question 28

the endothelium and coagulation system

Answer 28

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.

Question 29

what is the difference between meningitis and septicaemia

Answer 29

meningitis- bacteria in the cerebrospinal fluid that surrounds the brain and spine septicaemia- bacteria in the blood

Question 30

what is DIC

Answer 30

Disseminated intravascular coagulation is a syndrome of widespread intravascular activation of coagulation.

Question 31

what is petechiae

Answer 31

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

Question 32

tumbler test

Answer 32

the rash doesnt blanch when pressure is applied

Question 33

eccymoses

Answer 33

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.

Question 34

management of Neisseria meningitdis septicaemia

Answer 34

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

Question 35

mechanism of DIC

Answer 35

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.

Question 36

what is neissera menigitidis

Answer 36

gram negative cocci

Question 37

common causes of pneumonia

Answer 37

streptococcus pneumoniae haemophilus influenzae staphylococcus aureus

Question 38

lobar pneumonia

Answer 38

pulmonary consolidation demarcated by border of lung segment or lobe

Question 39

bronchopneumonia

Answer 39

patchy consolidation around the larger airways

Question 40

interstitial pneumonia

Answer 40

fine areas of shadowing in the lung fields and there is usually no sputum production at presentation

Question 41

clinical features of pneumonia

Answer 41

``` fever malaise tachypnea tahcycardia shock if severe ```