Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Y2 infection > sepsis and septic shock > Flashcards

sepsis and septic shock Flashcards

(47 cards)

Start Studying
1
Q

what is sepsis

A

systemic illness caused by microbial invasion of normally sterile parts of the body

SIRS + infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

traditional model of sepsis

A

SIRS
sepsis
severe sepsis
septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SIRS

A 
systemic inflammatory response syndrome 
temp >38 or <36
HR >90
RR >20 or PaCO2 <32
WBC >12 000 or <4000 or >10% bands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

severe sepsis

A

sepsis + end organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

septic shock

A

severe sepsis + hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define sepsis

A

life threatening organ dysfunction caused by dysregulated host response to infection

organ dysfunction - an acute change in total SOFA score >2 points consequent to the infection

SOFA score >2 reflects an overall mortality risk of ~10% in a general hospital pop w/ suspected infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define septic shock

A

sepsis w/ persisting hypotension requiring vasopressors to maintain MAP >65mmHg and serum lactate >2mmol/L despite adequate volume resus

pts w/ septic shock have a hospital mortality of 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does SOFA stand for

A

sequential (sepsis related) organ failure assessment score

respiration 
coagulation 
LFTs
BP 
GCS 
renal function - creatinine and urine output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

qSOFA

A

pts w/ suspected infection who are likely to have a prolonged ICU stay or die in hospital can be promptly identified w/ qSOFA

score ≥2 suggests greater risk of a poor outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what observations are measured in qSOFA

A

hypotension - systolic BP <100mmHg
altered mental status
tachypnoea - RR >22/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

importance of sepsis

A

common condition (30% of pts coming through acute medical assessment unit have some form of sepsis)

becoming more common (living longer, more co-morbidities etc)

increased morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

for every hrs delay in administering abx in septic shock, morality increases by …

A

7.6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the body’s defences to sepsis

A

physical - skin, mucosa, epithelial lining
innate immune system - IgA in GI tract, dendritic cells/macrophages
adaptive immune system - lymphocytes, immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

origin of sepsis

A

originates from a break of integrity of host barrier (physical or immunological)
organism enters the bloodstream creating a septic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pathophysiology of sepsis

A

uncontrolled inflammatory response

pts w/ sepsis have features consistent w/ immunosuppression

probable change of the sepsis syndrome over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the features consistent w/ immunosuppression in sepsis pts

A

loss of delayed hypersensitivity
inability to clear infection
predisposition to nosocomial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the change of the sepsis syndrome over time

A

initial increase in inflammatory mediators
shift towards an anti-inflammatory immunosuppressive phase
depends on the health of the patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 phases in pathogenesis of sepsis

A

release of bacterial toxins
release of mediators
effects of specific excessive mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

release of bacterial toxins

Study These Flashcards
A

bacterial invasion into body tissues is a source of dangerous toxins
may or may not be neutralised and cleared by existing immune system

20
Q

toxins released by gram -ve bacteria

Study These Flashcards
A

lipopolysaccharide (LPS)

21
Q

toxins released by gram +ve bacteria

Study These Flashcards
A

microbial associated molecular pattern (MAMP):
lipoteichoic acid
muramyl dipeptides

superantigens:
staphylococcal toxic shock syndrome toxin (TSST)
streptococcal exotoxins

22
Q

release of mediators in response to infection

Study These Flashcards
A

effects of infections due to endotoxin and exotoxin release

mediator role on sepsis

23
Q

endotoxin release

Study These Flashcards
A

LPS needs an LPS-binding protein to bind to macrophages

LTA don’t require these proteins

24
Q

exotoxin release

Study These Flashcards
A

pro-inflammatory response

small amounts of superantigens will cause a large amount of mediators to be secreted: cascade effect

25
mediator role in sepsis
2 types of mediators can be released: pro-inflammatory mediators - causes inflammatory response that characterises sepsis (too much of pro-inflammatory response can lead to septic shock and multiorgan failure and death) compensatory anti-inflammatory reaction - can cause immunoparalysis - uncontrolled infection and multi-organ failure
26
examples of pro-inflammatory mediators
TNF-alpha IL1 IFN-gamma
27
examples of anti-inflammatory mediators
IL-10 transforming growth factor-beta LPS-binding protein
28
effects of specific excessive mediators - pro-inflammatory mediators
promote endothelial cell - leukocyte adhesion released of arachidonic acid metabolites complement activation vasodilation of blood vessels by NO increased coagulation by release of tissue factors and membrane coagulants cause hyperthermia
29
effects of specific excessive mediators - anti-inflammatory mediators
inhibit TNF-alpha augment acute phase reaction inhibit activation of coagulation system provide -ve feedback mechanisms to pro-inflammatory mediators
30
what do the clinical features of sepsis depend on
host organism environment
31
features of organ dysfunction
CNS: altered consciousness, confusion, psychosis haematology: reduced platelets, increased PT/APTT, reduced protein c, increased D dimer resp: tachypnoea, PaO2 <70mmHg, sats <90% CVS: tachycardia, hypotension liver: increased liver enzymes, reduced albumin, increased PT kidney: oliguria, anuria, increased creatinine
32
general features of sepsis
fever >38C - chills, rigor, flushes, cold sweats, night sweats hypothermia <36C - esp in elderly, very young children and immunosuppressed tachycardia >90BPM tachypnoea >20/min altered mental status - es- elderly hyperglycaemia >8mmol/L in the absence of diabetes
33
inflammatory variables in sepsis
``` leucocytosis (WCC >12 000/ml) leucopenia (WCC <4000/ml) normal WCC w/ >10% immature forms high CRP high procalcitonin ```
34
haemodynamic variables in sepsis
``` artieral hypotension (systolic <90 or MAP <70) SvO2 >70% ```
35
organ dysfunction variables in sepsis
arterial hypoxaemia (PaO2/FiO2 <50mmHg) oliguria (<0.5ml/kg/h) creatinine increase compared to normal baseline coagulation abnormalities (PT >1.5 or APTT >60s) ileus thrombocytopenia (<150 000/ml) hyperbilirubinemia
36
tissue perfusion variables in sepsis
high lactate | skin mottling and reduced capillary perfusion
37
effect of host on sepsis presentation
age comorbidities (COPD, DM, CCF, CRF, disseminated malignancy) immunosuppression previous surgery - splenectomy
38
immunosuppression and sepsis presentation
acquired - HIV/AIDS drug induced - steroids, chemotherapeutic agents, biologics congenital - agammaglobulinaemia phagocytic defects, defects in terminal complement component
39
effect of organism on presentation of sepsis
gram +ve/-ve virulence factors (e.g. MRSA, toxin secretion, ESBL, KPC, NDM-1) bioburden
40
effect of environment on presentation of sepsis
occupation travel hospitalisation
41
Sepsis 6
2A2B2C take 3, give 3 blood cultures blood lactate measure urine output oxygen - aims sats 94-98% IV abx IV fluid challenge
42
why do we carry out blood cultures blood lactate measure urine output
blood cultures - make microbiological diagnosis (30-50% +ve), if spike in temp take 2 sets lactate - marker of generalised hypoperfusion/severe sepsis/poorer prognosis low urine output - marker of renal dysfunction
43
how to choose what abx to use
based on working diagnosis from hx and examination local abx guidelines consider: allergy, previous MRSA/ESBL/CPE, abx toxicity/interactions
44
types of lactate
type A - hypoperfusion | type B - mitochondrial toxins, alcohol, malignancy, metabolism errors
45
IV fluids
30ml/kg fluid challenge | 2.1L for 70kg patient
46
when to consider HDU referral
``` low BP responsive to fluids lactate >2 despite fluid resus elevated creatinine oliguria liver dysfunction - Bil, PT, Plt bilateral infiltrates, hypoxaemia ```
47
when to consider ITU
septic shock multi-organ failure requires sedation, intubation and ventilation

Y2 infection (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions