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Microbiology > Sepsis > Flashcards

Sepsis Flashcards

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1
Q

What does SIRS mean?

A

Systemic inflammatory response syndrome.
Various causes not just infection.

A set of clinical features that may indicate infection.

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2
Q

Symptoms of SIRS

A

Temp >38 or <36
HR >90 bpm
RR >20/min or PaCO2 <4.3 kPa

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3
Q

Sepsis

A

SIRS + infection

Infection with features indicating significant risk of deterioration/death.
Benefit from early antibiotics.

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4
Q

Septic shock

A

Sepsis with hypotension not corrected by fluid resuscitation.

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5
Q

Bacteraemia

A

Circulation of bacteria in the blood.

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6
Q

Septicaemia

A

Blood poisoning, especially that caused by bacteria or their toxins

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7
Q

Clinical syndromes causing sepsis

A

Pneumonia > intra-abdominal > UTI > other

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8
Q

Bugs causing community acquired sepsis

A

Strep. pneumoniae
Strep. pyogenes
Stap. aures
E. coli

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9
Q

Bugs causing healthcare-associated sepsis

A

S. aures

E.coli

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10
Q

Host risk factors for sepsis

A 
Increased risk of acquiring infection.
Impaired immune response.
Pre-existing organ dysfunction.
Extremes of age.
Genetic factors.
Timeliness of treatment.
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11
Q

Environmental factors that increase risk of infection

A

Hygiene

Sanitation

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12
Q

Conditions that increase risk of infection

A

COPD: inc respiratory infections

Lymphoedema: inc soft tissue infections

Urethral catheter: inc urinary tract infections

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13
Q

Factors causing impaired immune response

A

Congenital immunodeficiency syndromes.
HIV/AIDs.
Splenectomy, functional hyposplenism.
Iatrogenic (chemotherapy or immunosuppressant drugs).
Chronic conditions (malignancy, diabeter, malnutrition).

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14
Q

Why are extremes of age vulnerable to sepsis?

A

Old: immune senesence, comorbidity

Yourn: immature immunity, limited physiological reserve

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15
Q

Gender more at risk of sepsis

A

Male

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16
Q

Initiation of innate immune response

A

Pattern recognition receptors (PRRs) on leukocytes recognise PAMPs and DAMPs/alarmins.
PRR activation causes cytokine release (TNFalpha, IL-1, IL-8) which leads to fever, tachycardia, leukocytosis, acute-phase response (high CRP and procalcitonin).

Cascade of leukocyte, complement and coagulation activation.

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17
Q

PAMP

A

Pathogen associated molecular pattern

Structures are highly conserved among microbes.
e.g peptioglycan, LPS, lipoteichoic acid, fermylmethionine, flagellin.

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18
Q

DAMP

A

Damage associated molecular patterns/alarmins

Endogenous molecules released from injured cells (DNA, RNA, histones).
Also released in sterile injury.

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19
Q

What are bacterial ‘super-antigens’

A

Things that directly trigger cytokine release from T-cells.

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20
Q

Examples of bacterial ‘super-antigens’

A

Staphylococcaltoxic shock syndrome from toxic shock syndrome toxin-1 (TSST-1).
Streptococcal toxic shock syndrome with erythrotoxins.
Fulminant septic shock often with erythematous rash.

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21
Q

Causes of acute organ dysfunction associated with sepsis

A 
Tissue hypoperfusion (vasodilation, dysregulated perfusion, hypotension).
Vascular endothelial dysfunction (loss of barrier function, interstitial oedema, intravascular hypovolaemia).
Mitochondrial dysfunction (oxidative stress).
Impaired tissue oxygenation (leads to tissue death and further inflammation released).
Impaired coagulation (tissue factor release, decrease in anti-coagulants, increase in fibrin leading to microvascular thrombosis/DIC).
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22
Q

Mechanism of ARDS

A

Acute respiratory Distress Syndrome

Non-cardiogenic pulmonary oedema.
Increased vascular permeability.
Hypoxaemia and bilateral pulmonary infiltrates.

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23
Q

Mechanism of cardiovascular collapse (spetic shock)

A

Vasodilation (e.g endotoxin).
Hypotension.
Tissue hypoperfusion (inc lactate).
Myocardial damage/impairment (inc troponin).

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24
Q

Mechanism of AKI

A

Acute Kidney Injury

Hypotension +/- hypovolaemia.
Direct inflammatory injury.

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25
Q

GI condition that increases liklihood of sepsis

A 
Paralytic ileus (muscles not working) can cause a blockage.
Possible leak of organisms/toxins into circulation.
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26
Q

Clinical presentation of sepsis

A 
Shivering, fever, very cold
Extreme pain or general discomfort ('worst ever')
Pale or discolored skin
Sleepy/difficult to wake up, confused
I feel like I might die
SOB
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27
Q

Red Flag sepsis signs

A

INFECTION + one of:

  • HR >130
  • SBP <90 (MAP<65, decrease SBP by >40)
  • RR >25
  • Oxygen sat <92% or need more that 40% FiO2 to maintain it
  • Lactate >2
  • New altered mental state
  • Purpuric rash, mottled/ashen
  • Cyanosed skin, lips or tongue
  • Poor urine output (not passed urine >18hr or <0.5 ml/kg/hr)
  • Non-blanching rash
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28
Q

Sepsis 6

A 
Blood cultures
Urine output
Fluids
Antibiotics
Lactate
Oxygen (keep above 94%)
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29
Q

False negative

A

Patient has condition X but test tells you they don’t. Sensitivity

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30
Q

False positive

A

Patient doesn’t have condition X but test tells you they do. Specificity

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31
Q

Positive predictive value

A

Given a positive test result how likely is the patient to have the disease.

32
Q

Negative predictive value

A

Given negative test result how likely is the patient not to have disease.

33
Q

Examples of sterile sites

A 
CSF
Blood/bone marrow
Lower respiratory tract
Bladder/kidneys
Bone/joints
Pleura/peritoneum
Most surgical specimens
34
Q

Examples of non-sterile sites

A 
Mouth/nasopharynx
Upper respiratory tract
Skin
GI tract
Urethra
Female GU tract
35
Q

Gram stain

A

Stain with crystal violet and fix with iodine.
Elude the blue stain with acetone for 2 seconds. Thin peptidoglycan wall (gram negative) allows stain to leech out.
Counterstain with a red dye, such as neutral red or carbol fuschin.

36
Q

Non-spore forming gram positive

A

Listeria

Corynebacterium

37
Q

Spore forming gram positive

A

Clostridium

Bacillus

38
Q

Facultative anaeroes

A

Prefer aerobic respiration but can switch to anaerobic fermentation.

e.g Staphylococcus spp, streptococcus spp, E.coli

39
Q

Obligate aerobes

A

Require oxygen

e.g pseudomonas, mycobacterium tuberculosis

40
Q

Obligate anaerobes

A

Killed by oxygen.

e.g bacteriodes, clostridium spp

41
Q

Microaerophillic

A

Require small amount of oxygen to survive 2-10%.

e.g camphlobacter spp.

42
Q

MacConkey agar

A

Bile salts (suppress most gram +ves).
Lactose (Nutrition source for lactose fermenters-> pH lowers).
Peptone (Nutrition source for non-lactose fermenters-> pH increases).
Neutral red (Turns pink as pH lowers).

43
Q

Catalase test

A

hydrogen peroxide turned to water and oxygen within seconds if enzyme present.

44
Q

Coagulase test

A

Fibrinogen to fibrin (4 hours).

45
Q

Things that Staph. aures causes

A

Skin and soft tissue infections.
Endocarditis
Septic arthritis
Osteomyelitis

46
Q

First line treatment for MSSA

A

flucloxacillin

47
Q

First line treatment for MRSA

A

Vancomycin

48
Q

ESBL

A

Extended spectrum beta lactamase

49
Q

CPE

A

Carbapenemase producing enterobacteriacae

50
Q

Enterobacteriacae

A

Gut commensals, grow on MacConkey agar.

e.g
E.coli (UTI, biliary sepsis, neonatal meningitis)
Klebsiella (UTI, biliary, LRTI)
Enterobacter (HAI)
Salmonella
Non-typhoidal (gastroenteritis, sepsis, osteomyelitis)
S.typhi/paratyphi (enteric fever)

51
Q

What causes a green film, HAI?

A

Pseudomonas aeruginosa

52
Q

acute-phase response markers

A

high CRP and procalcitonin

53
Q

What does cytokine release cause?

A

fever
tachycardia
leukocytosis
acute-phase response

54
Q

Definition of severe sepsis

A

sepsis + end-organ damage

55
Q

Definition of endovascular infection

A

Infection of vascular endothelium; either arterial or venous

56
Q

Definition of endocarditis

A

Endovascular infection involving the

heart (either heart valves and/or endocardium)

57
Q

Infective endarteritis

A

Infection of arterial endothelium, most commonly aorta

58
Q

Risk factors for endocarditis

A

• Prosthetic heart valves
– Increased risk with metal valves and 1st yr after implantation
– Overall risk: 1% per patient per year
• Congenital / rheumatic heart disease
– Not isolated MVP/ASD
– Mitral > Aortic > Triscuspid > Pulmonary
• Previous history of endocarditis
• PWID
• Haemodialysis / long lines
• Poor dentition

59
Q

PWID

A

People who use IV drugs

60
Q

Pathological features of endocarditis

A 
• Damaged endothelium
  – Platelet and fibrin deposition
  – Bacteria in bloodstream may adhere
e.g. fibronectin binding of S. aureus
• Local damage
 – Leaky valves
 – Ruptured chordae
 – Ring abscesses
 – ‘Ball-valve’ obstruction
• Distant emboli
• Sepsis syndrome
61
Q

Clinical features of endocarditis

A

• Often non-specific, ‘grumbling’: malaise, fever/sweats, anorexia, weight loss
• Symptoms usually start within 2 weeks of bacteraemia
– More acute with Staph aureus
• Indolent cases
– ‘Subacute bacterial endocarditis’ (SBE)
– Usually lower grade pathogens (coagulase negative staphylococci, Strep viridans)
• May present acutely with sepsis / cardiac failure / multiorgan failure
– Medical and/or surgical emergency
• Embolic phenomena (brain, lungs, peripheries)
• Vasculitic / immunological phenomena

62
Q

Features of left-sided endocarditis (embolic)

A

Infarction (stroke)
Brain abscess
Splinter haemorrhage
Janeway lesions (flat, haemorrhagic, painless)

63
Q

Features of right-sided endocarditis (embolic)

A

Lung abscess

Multiple septic emboli in lungs

64
Q

Investigations for endocarditis

A
  • Multiple sets of blood cultures (off antibiotics)
  • TTE
  • TOE
65
Q

What does TTE stand for?

A

Trans-thoracic echo (TTE):

identifies 50-60% of endocarditis

66
Q

What does TOE stand for?

A

Trans-oesophageal echo (TOE):

identifies 90% of endocarditis

67
Q

Causitive agents of endocarditis

A 
Staphylococci (42%)
   -S. aureus
   -Coagulase-negative Staph (CoNS)
Streptococci (34%)
   -Strep viridans (alphaa haem strep)
   -Streptococcus bovis
Enterococci (8%)
   E. faecalis; E. faecium
‘HACEK’ organisms (3%)
Streptococcus pneumoniae (1%)
Other bacteria (<1%)
Fungi (< 0.5%)
Culture negative endocarditis (6%)
68
Q

HACEK

A 
Haemophilus
Actinobacillus / Aggregatibacter
Cardiobacterium
Eikenella
Kingella
69
Q

Causes of culture-negative endocarditis

A

Approx 5% of cases

Antibiotics
Fastidious/difficult to culture organisms:

– Coxiella burnetti (Q fever)
– Chlamydia sp
– Bartonella sp
– Legionella
– Mycoplasma
70
Q

Treatment of endocarditis caused by viridans streptococci

A
  • 4 weeks of benzylpenicillin (penicillin G)

- together with 2 weeks of gentamicin

71
Q

Treatment of endocarditis caused by enterococci

A
  • 4 weeks of amoxicillin (or vancomycin)

- together with 2 weeks of gentamicin

72
Q

Treatment of endocarditis caused by coagulase-negative staphylococci

A

6 weeks vancomycin

73
Q

What should you do to monitor for the development of complications of endocartitis?

A
  • Regular ECG
  • Repeat echocardiogram
  • Audiometry if receiving regular gentamicin
  • Renal function / monitor eGFR
  • LFTs if on high dose beta lactam / rifampicin
74
Q

What is arteritis?

A

The inflammation of walls of arteries

75
Q

What is infective endarteritis?

A

Bacterial or other infection of intima layer of arteries.

76
Q

Bacteria causing infective endarteritis

A

Salmonella and E.coli common in aorta

Staphylococcus aures in other vessels

Microbiology (4 decks)

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