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Infection > Session 3- Sepsis, Meningitis and Adaptive Immunity > Flashcards

Session 3- Sepsis, Meningitis and Adaptive Immunity Flashcards

1
Q

what is sepsis

A

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

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2
Q

what causes sepsis

A

vasodilation
capillary leakage
amplification of the immune system

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3
Q

clinical features of infection

A 
rubor 
calor
dolor
tumour 
loss of function
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4
Q

respiratory physiological features of sepsis

A

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

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5
Q

cardiac physiological features of sepsis

A

low BP

tachycardia and end organ damage

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6
Q

CNS physiological features of sepsis

A 
reduced blood perfusion to brain
confusion
drowsiness
slurred speech
agitation
anxiety
reduced level of consciousness
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7
Q

renal physiological features of sepsis

A

reduced renal output

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8
Q

management of sepsis

A

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

out: blood cultures, lactate and Hb, urine output

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9
Q

naiive t cells

A

havent seen the antigen before

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10
Q

effector cells

A

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

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11
Q

where are APCs found

A 
Mucosal membranes
skin
blood- plasmacytoid cells
lymph nodes
spleen
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12
Q

what do APCs do

A

they present pathogen antigenic peptide attached ti MHC.

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13
Q

where are MHC II expressed

A

dendritic cells
b cells and macrophages

they present microbial peptides from extracellular micobes

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14
Q

where are MHC I expressed

A

all nucleated cells and present microbial peptides from intracellular microbes.

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15
Q

endogenous pathway

A
  • 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
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16
Q

exogenous pathway

A
  • 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
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17
Q

what are the three main layers - meninges

A

pia mater- closest to the brain and spinal cord

arachnoid- in the middle

dura mater- outermost layer

18
Q

what is meningitis

A

inflammation of the meningeal lining of the brain and spine

19
Q

what bacteria cause meningitis

A

Neisseria meningitidis
streptococcus pneumoniae
haemophilus influenzae

20
Q

viruses that cause meningitis

A

enterovirus - echoviruses

21
Q

fungi that cause meningitis

A

crytococcus neoformans

22
Q

clinical features of meningitis

A

general infection features

headache
photophobia
vomiting 
neck stiffness on flexion of neck
irritable
23
Q

septic shock

A

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

24
Q

causative agents of sepsis

A

gram-negative infections

25
Q

investigations of sepsis

A

obtain samples for microbiology
blood cultures
urine sample
CSF sample

26
Q

management of sepsis

A 
give high flow oxygen 
take blood cultures 
give IV antibiotics
Give a fluid challenge 
measure lactate 
measure urine output
27
Q

treatment of sepsis

A

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.

28
Q

the endothelium and coagulation system

A

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.

29
Q

what is the difference between meningitis and septicaemia

A

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

septicaemia- bacteria in the blood

30
Q

what is DIC

A

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

31
Q

what is petechiae

A

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

32
Q

tumbler test

A

the rash doesnt blanch when pressure is applied

33
Q

eccymoses

A

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.

34
Q

management of Neisseria meningitdis septicaemia

A

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

35
Q

mechanism of DIC

A

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.

36
Q

what is neissera menigitidis

A

gram negative cocci

37
Q

common causes of pneumonia

A

streptococcus pneumoniae
haemophilus influenzae
staphylococcus aureus

38
Q

lobar pneumonia

A

pulmonary consolidation demarcated by border of lung segment or lobe

39
Q

bronchopneumonia

A

patchy consolidation around the larger airways

40
Q

interstitial pneumonia

A

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

41
Q

clinical features of pneumonia

A 
fever
malaise 
tachypnea
tahcycardia
shock if severe

Infection (14 decks)

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