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C. Year 3: SBOM > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

What is sepsis?

1 - bacterial infection causing local inflammation
2 - viral infection causing local inflammation
3 - infection causing widespread and systemic inflammation
4 - bacteria present in the blood without inflammation

A

3 - infection causing widespread and systemic inflammation

  • form of the systemic inflammatory response syndrome
  • can be life threatening causing organ dysfunction
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2
Q

What is septic shock?

1 - sepsis subset caused by cellular/circulatory and metabolic abnormalities that increase mortality
2 - sepsis subset where only immunocompromised patients are affected
3 - sepsis subset that caused neurological dysfunction
4 - sepsis subset linked to fungal infections

A

1 - sepsis subset caused by cellular/circulatory and metabolic abnormalities that increase mortality

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3
Q

How many people worldwide and in the UK have sepsis?

1 - >10 million worldwide and 100,000 in the UK
2 - >30 million worldwide and 100,000 in the UK
3 - >30 million worldwide and 250,000 in the UK
4 - >10 million worldwide and 250,000 in the UK

A

3 - >30 million worldwide and 250,000 in the UK

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4
Q

What is the current mortality rate of sepsis in community and in hospitals?

1 - community is 40-50% and hospital <10%
2 - community is 10-20% and hospital >10%
3 - community is 20-30% and hospital >40%
4 - community is 20-30% and hospital <10%

A

3 - community is 20-30% and hospital >40%

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5
Q

How many deaths in the UK each year are due to sepsis?

1 - 10-20,000
2 - 20-30,000
3 - 30-40,000
4 - 40-70,000

A

4 - 40-70,000

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6
Q

What is the leading cause of ICU death?

1 - diabetes
2 - sepsis
3 - cancer
4 - transplants

A

2 - sepsis

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7
Q

What triggers the initiation of the inflammatory response of the body?

1 - PRRs binding to antigens of microbials
2 - damage to endothelium
3 - damage to an organ
4 - a specific organ is damaged

A

1 - PRRs binding to antigens of microbials

  • pattern recognition receptors identify foreign pathogens
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8
Q

Once PRR have recognised pathogens in the circulation they initiate an inflammatory immune response. The response of the host is to activate 2 specific innate immune cells. Which cells are these?

1 - B cells and macrophages
2 - T cells and macrophages
3 - dendritic cells and neutrophils
4 - neutrophils and macrophages

A

4 - neutrophils and macrophages

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9
Q

Once PRR have recognised pathogens in the circulation they initiate an inflammatory immune response, activating neutrophils and macrophages. These in-turn are able to produce which cytokines?

1 - TNF, IL-6, IL-12, and IL-8,
2 - IL-1, IL-4, IFN-γ, IL-12, and IL-18,
3 - TNF, IL-1, IFN-γ, IL-2, and IL-10,
4 - TNF, IL-1, IFN-γ, IL-12, and IL-18

A

4 - TNF, IL-1, IFN-γ, IL-12, and IL-18

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10
Q

Once PRR have recognised pathogens in the circulation they initiate an inflammatory immune response, activating neutrophils and macrophages, which can then secrete cytokines TNF, IL-1, IFN-γ, IL-12, and IL-18. Alongside ROS, prostaglandins and platelet activating factor endothelium secrete adhesion molecules and the complement pathway is activated. This pro-inflammatory state is able to directly activate the intrinsic pathway of the coagulation cascade. Which factor is activated by the pro-inflammatory state, that in turn begins the coagulation cascade?

1 - factor IIa
2 - factor VII
3 - factor XII
4 - factor V

A

3 - factor XII

This begins the extrinsic pathway

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11
Q

In the pro-inflammatory condition what can happen to the endothelium?

1 - secrete anti-inflammatory cytokines
2 - thicken due to the stress
3 - pulmonary embolism occurs
4 - become damaged and leaky

A

4 - become damaged and leaky

  • means nutrients cannot be delivered to cells and waste cannot be removed effectively.
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12
Q

In the pro-inflammatory condition the endothelium becomes damaged and leaky. What happens to the endothelium meaning they become leaky?

1 - cytokines loosen tight junctions
2 - cytokines induce cellular apoptosis
3 - cytokines cause endothelium hyperplasia
4 - cytokines do not affect endothelium

A

1 - cytokines loosen tight junctions

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13
Q

In the pro-inflammatory condition the endothelium becomes damaged and leaky. Endothelium cells also increase the release of nitric oxide, which then does what to the blood vessels?

1 - cause vasoconstriction and increased BP
2 - cause vasoconstriction and reduced BP
3 - cause vasodilation and increased BP
4 - cause vasodilation and reduced BP

A

4 - cause vasodilation and reduced BP

  • main cause of hypotension in sepsis patients
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14
Q

What are the 4 key features that are present due to the pro-inflammatory state?

1 - fever, coagulopathy, vasodilation, capillary leaking
2 - fever, anti-coagulopathy, vasodilation, capillary leaking
3 - fever, coagulopathy, vasoconstriction, capillary leaking
4 - hypothermia, coagulopathy, vasodilation, capillary leaking

A

1 - fever, coagulopathy, vasodilation, capillary leaking

  • fever = cytokines signal to hypothalamus to increase body temperature (typically IL-1)
  • inflammation initiates coagulation cascade
  • nitric oxide and cytokines induce vasodilation
  • capillary leaking is due to relaxed/damaged tight junctions and increased fluid
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15
Q

In patients who have sepsis there is an attenuation of of endothelial produced anti-coagulant factors by inflammatory markers. What anti-coagulant factors are attenuated, meaning the coagulation cascade can go unchecked?

1 - tissue factor pathway inhibitor and protein S
2 - tissue factor pathway inhibitor,
thrombomodulin, and protein S
3 - tissue factor pathway inhibitor,
thrombomodulin, and protein C
4 - thrombomodulin, and protein C

A

3 - tissue factor pathway inhibitor,
thrombomodulin, and protein C

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16
Q

In patients who have sepsis there is an attenuation of of endothelial produced anti-coagulant factors tissue factor pathway inhibitor, thrombomodulin, and protein C. pro-inflammatory markers are also able to influence fibrinolysis (breakdown of fibrin). Is fibrinolysis increased or decreased?

A
  • fibrinolysis is decreased
  • caused by increased plasminogen activator inhibitor-1 expression
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17
Q

Vasodilation and leaky endothelium results in interstitial oedema and reduced blood flow in small blood vessels. This can cause stasis and diminished removal of waste and coagulation factors. This combined with increased coagulator state and fibrin deposits causes what to occur to perfusion levels in tissues?

1 - tissue perfusion increases
2 - tissue perfusion decreases

A

2 - tissue perfusion decreases

  • coagulation continues
  • fibrin rich deposits in blood vessels
  • overuse of coagulation factors can even cause haemorrhage
  • referred to as Disseminated Intravascular Coagulation
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18
Q

What is cardiogenic shock?

1- heart continues to pump enough blood and oxygen but does not reach brain and other vital organs
2 - heart unable to pump enough blood and oxygen but still reaches the brain and other vital organs
3 - heart unable to pump enough blood and oxygen to the brain and other vital organs
4 - heart shuts down

A

3 - heart unable to pump enough blood and oxygen to the brain and other vital organs

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19
Q

There are 3 stages to cardiogenic shock in sepsis. What is the first stage?

1 - cold peripheries, cardiac myocyte suppression with a high filling pressure (not fluid responsive)
2 - distributive shock (warm peripheries) with peripheral vasodilatation
3 - immunocompromised and endothelium damage
4 - hypovolaemic shock (cold peripheries) due to capillary leakage, peripheral and pulmonary oedema and a low filling pressure (fluid responsive)

A

2 - distributive shock (warm peripheries) with peripheral vasodilatation

  • vasodilation is due to pro-inflammatory markers and nitric oxide release from endothelium
  • enough fluid in vessels to not cause hypovolaemia
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20
Q

There are 3 stages to cardiogenic shock in sepsis. What is the second stage?

1 - cold peripheries, cardiac myocyte suppression with a high filling pressure (not fluid responsive)
2 - distributive shock (warm peripheries) with peripheral vasodilatation
3 - immunocompromised and endothelium damage
4 - hypovolaemic shock (cold peripheries) due to capillary leakage, peripheral and pulmonary oedema and a low filling pressure (fluid responsive)

A

4 - hypovolaemic shock (cold peripheries) due to capillary leakage, peripheral and pulmonary oedema and a low filling pressure (fluid responsive)

  • giving fluid can help with this
  • mottled skin
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21
Q

There are 3 stages to cardiogenic shock in sepsis. What is the third stage?

1 - cold peripheries, cardiac myocyte suppression with a high filling pressure (not fluid responsive)
2 - distributive shock (warm peripheries) with peripheral vasodilatation
3 - immunocompromised and endothelium damage
4 - hypovolaemic shock (cold peripheries) due to capillary leakage, peripheral and pulmonary oedema and a low filling pressure (fluid responsive)

A

1 - cold peripheries, cardiac myocyte suppression with a high filling pressure (not fluid responsive)

  • giving fluid will not help with this
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22
Q

There are 3 stages to cardiogenic shock in sepsis. The 1st stage is distributive shock (warm peripheries) with peripheral vasodilatation. Which of the following is NOT a neurohumeral (sympathetic) mechanism to help maintain cardiac output, blood pressure and tissue perfusion?

1 - baroreceptor reflexes
2 - catecholamine release
3 - atrial natriuretic peptide
4 - renin-angiotensin axis
5 - increased sympathetic activation
6 - ADH release

A

3 - atrial natriuretic peptide

  • works to reduce fluid levels
  • aim is to reduce the stress on the heart
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23
Q

There are 3 stages to cardiogenic shock in sepsis. The 1st stage is distributive shock (warm peripheries) with peripheral vasodilatation. Neurohumeral (sympathetic) mechanism to help maintain cardiac output, including baroreceptor reflexes, catecholamine release, renin-angiotensin axis, increased sympathetic activation and ADH release. What physiological response does this then present in for the patient?

1 - tachycardia, peripheral vasoconstriction,
and renal conservation of fluid, pallor of the skin
2 - bradycardia, peripheral vasodilation,
and renal conservation of fluid, pallor of the skin
3 - tachycardia, peripheral vasoconstriction,
and renal conservation of fluid, rubor of the skin
4 - bradycardia, peripheral vasoconstriction,
and renal conservation of fluid, pallor of the skin

A

1 - tachycardia, peripheral vasoconstriction,
and renal conservation of fluid, pallor of the skin

  • HOWEVER, septic shock can initially cause cutaneous vasodilation and thus present with warm, flushed skin
  • coronary and cerebral blood flow remains constant as not affected by sympathetic tone as much
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24
Q

There are 3 stages to cardiogenic shock in sepsis. The 1st phase is distributive shock (warm peripheries) with peripheral vasodilatation. If this is not corrected hypovolaemic shock with cold peripheries and low filling pressure which is fluid responsive follows. There is also widespread hypoxia causing what to occur?

1 - anaerobic respiration with no lactate production
2 - aerobic respiration with no lactate production
3 - anaerobic glycolysis and excessive lactate production
4 - aerobic glycolysis with no lactate production

A

3 - anaerobic glycolysis and excessive lactate production

  • high lactate causes metabolic lactic acidosis
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25
Q

There are 3 stages to cardiogenic shock in sepsis. The 1st phase is distributive shock (warm peripheries) with peripheral vasodilatation. If this is not corrected hypovolaemic shock with cold peripheries and low filling pressure which is fluid responsive follows. There is also widespread hypoxia causing anaerobic glycolysis and excessive lactate production. This in turn results in what to occur to blood vessels?

1 - impaired vasomotor response and oedema
2 - increase vasomotor response and impaired perfusion
3 - impaired vasomotor response and increase cardiac output
4 - increase vasomotor response and increased cardiac output

A

1 - impaired vasomotor response and oedema

  • cardiac output is impaired causing low filling pressure
  • endothelial cells at risk for developing anoxic injury
  • widespread tissue hypoxia and tissue and organ failure
26
Q

The 3rd stage of cardiogenic chock that occurs during sepsis is when:

  • a patient has cold peripheries,
  • cardiac myocyte suppression
  • high filling pressure (not fluid responsive
A
27
Q

During sepsis what happens to glucose control?

1 - increased insulin sensitivity and reduced blood glucose
2 - increase insulin resistance and increases blood glucose
3 - reduced insulin sensitivity and reduced blood glucose
4 - reduced insulin resistance and hyperglycaemia

A

2 - increased insulin resistance and increases blood glucose
- less insulin released
- GLUT4dozsnt work so glucose is not absorbed effectively

28
Q

During sepsis what happens to glucose control?

1 - increased insulin sensitivity and hypoglycaemia
2 - increase insulin resistance and hyperglycaemia
3 - reduced insulin sensitivity and hypoglycaemia
4 - reduced insulin resistance and hyperglycaemia

A

2 - increased insulin resistance and increases blood glucose

  • insulin release is impaired
  • GLUT 4 is impaired
29
Q

During sepsis there is increased insulin resistance and hyperglycaemia, which gluconeogenesis also contributes to. Which of the following does not drive gluconeogenesis?

1 - glucagon
2 - cortisol
3 - growth hormone
4 - T3 and T4

A

4 - T3 and T4

  • increase GLUT2 receptors in liver so increase insulin sensitivity
  • thyroid hormone release would have the opposite effect
30
Q

Vasodilation and leaky endothelium results in interstitial oedema and reduced blood flow in small blood vessels. This can cause stasis and diminished removal of waste and coagulation factors. This combined with increased coagulator state and fibrin deposits causes reduced tissue perfusion called Disseminated Intravascular Coagulation. What effect does this have on the adrenal gland?

1 - adrenal gland hyperplasia
2 - adrenal gland hypertrophy
3 - adrenal gland necrosis

A

3 - adrenal gland necrosis

  • glucocorticoid levels drop
31
Q

Which of the following is NOT included in the things to look for if we think a patient has sepsis:

1 - pyrexia (fever)
2 - neutrophilia (high neutrophil number)
3 - rash
4 - lung consolidation
5 - dysuria (painful urination)
6 - peritonitis (inflamed peritoneum)
7 - anaphylaxis

A

7 - anaphylaxis

32
Q

The Sequential Organ Failure Assessment (SOFA) score is a tool used to assess the risk of mortality using multiple measures. A change of what in the SOFA score suggests sepsis?

1 - increase of >1 point
2 - increase of >2 point
3 - increase of >3 point
4 - increase of >4 point

A

2 - increase of >2 point

33
Q

Patients with septic shock can be identified with a clinical construct. What do we use as the diagnosis for blood pressure?

1 - hypertension >180mmHg
2 - hypertension >150mmHg
3 - hypotension with MAP <65mmHg
4 - hypotension <90mmHg

A

3 - hypotension with MAP <65mmHg

  • even with the use of vasopressors (increase BP)
    MAP = (2 x DBP) + SBP) / 3
34
Q

Patients with septic shock can be identified with a clinical construct. What do we use as the diagnosis for blood lactate?

1 - serum lactate >2mmol despite fluid resuscitation
2 - serum lactate >6mmol despite fluid resuscitation
3 - serum lactate >8mmol despite fluid resuscitation
4 - serum lactate >12mmol despite fluid resuscitation

A

1 - serum lactate >2mmol despite fluid resuscitation

35
Q

When we look at a patient who is suspected of having sepsis, what would we expect to see in their breathing?

1 - tachypnea
2 - bradypnea
3 - hyperventilation
4 - hypoventilation

A

1 - tachypnea

36
Q

When we look at a patient who is suspected of having sepsis, we might expect to see tachypnea (increased breathing rate). Which of the following is not a normal sign we would see in the breathing of a patient with suspected sepsis?

1 - use of accessory muscles
2 - seesawing of chest and abdomen
3 - deviated trachea
4 - intercostal recession
5 - only able to speak a few words

A

3 - deviated trachea

37
Q

Acute Lung Injury (ALI) and Acute respiratory distress syndrome are often the 1st signs of sepsis.

A

Additional fluid in the lungs is due to leaking capillaires

38
Q

Staphlococcus aureus is a gram+ bacteria that is able to synthesise and secrete exotoxins. These exotoxins function as superantigens, with Toxic Shock Syndrome Toxin 1 (TSST-1 an 2) as examples. What do the super-antigens then do to T cells?

1 - bind specifically to MHC-I and II receptors on antigen presenting cells
2 - bind specifically to CD4 and CD8 cells
3 - bind non-specifically to any T cells
4 - bind specifically to B cells

A

3 - bind non-specifically to any T cells

39
Q

Staphlococcus aureus is a gram+ bacteria that is able to synthesise and secrete exotoxins. These exotoxins function as superantigens, with Toxic Shock Syndrome Toxin 1 (TSST-1 an 2) as examples. These super-antigens then bind non-specifically to any T cells, which can activate over 20% of T cells in the body. Why is this activation of T cells a bad thing?

1 - leads to overactive immune response
2 - leads to T cells binding with host cells
3 - leads to T cells activating B cells

A

1 - leads to overactive immune response

  • sepsis is defined as an over reaction to an immune response
  • huge inflammatory response follows due to cytokine release
  • means that T cells are unable to bind to the antigen on the pathogen
40
Q

Staphlococcus aureus is one of the top 5 hospital acquired infections and is commonly associated with antibiotic resistance. How does this bacteria induce sepsis?

1 - bind and activates B cells
2 - produced protein toxins that bind inactivate antibodies
3 - produce LPS that initiates system inflammation
4 - binds to endothelium creating biofilms

A

2 - produced protein toxins that bind and inactivate antibodies

  • cause toxic shock syndrome
41
Q

What % of hospital ICU patients is accounted for by severe sepsis or septic shock due to gram+ bacteria?

1 - 10%
2 - 30%
3 - 50%
4 - >80%

A

3 - 50%

  • S. aureus is the leading cause of sepsis among gram-positive bacteria
42
Q

The peptidoglycan (PG) and lipoteichoic acids (LTA) of Staphlococcus aureus is recognised by what pattern recognition receptor?

1 - toll like receptors
2 - NOD like receptors
3 - C type lectin receptors

A

1 - toll like receptors

  • specifically toll-like receptor 2 (TLR2)
43
Q

The peptidoglycan (PG) and lipoteichoic acids (LTA) of Staphlococcus aureus is recognised by toll like receptor-2 (TLR-2). What cell of innate immune system contain the TLR-2?

1 - macrophages
2 - B cells
3 - neutrophils
4 - mast cells

A

1 - macrophages

  • induces inflammatory responses due to activation of nuclear factor kappa B (NFκB) whose aim is to eradicate Staphlococcus aureus. They can therefore be used as markers of infection
44
Q

Exotoxins can be proteins or lipids and are a form of toxin produced by microorganisms, especially gram positive bacteria. What can exotoxins produced by bacteria cause?

1 - inflammation
2 - trigger innate immune response
3 - toxic shock syndrome
4 - cancer

A

3 - toxic shock syndrome

45
Q

Which of the following is NOT a sepsis red flag?

1 - Someone is concerned about sepsis
2 - Evidence of organ dysfunction
3 - Recent chemotherapy or neutropenic
4 - NEWS2 score is 7 or above
5 - Recent course of antibiotics

A

5 - Recent course of antibiotics

46
Q

If you suspect a patient has sepsis, which of the following is not one of the sepsis 6 that you must do in the 1st hour?

1 - give high flow oxygen
2 - measure lactate
3 - take blood cultures
4 - monitor ECG
5 - give antibiotics
6 - give a fluid challenge
7 - measure urine output

A

4 - monitor ECG

  • mnemonic BUFALO can help remember this
  • antibiotic used should be broad spectrum and given >1 hour
47
Q

There are 4 main causes of shock that the body can undergo. Which of the 4 below is sepsis generally associated with?

1 - cardiogenic
2 - hypovolaemic
3 - distributive
4 - obstructive

A

3 - distributive

48
Q

Systemic Inflammatory Response Syndrome (SIRS) is an exaggerated defence response of the body to a noxious stressor. Which of the following is not one of the four criteria used to identify a patient with SIRS?

1 - Temp >38oC or <36oC
2 - Heart Rate > >90 beats/min
3 - Respiratory Rate > 20 breaths/min
4 - Lactate >2mmol/L
5 - White Cell Count > 12/mm3 or < 4/mm3

A

4 - Lactate >2mmol/L

49
Q

Why can sepsis lead to cachexia?

1 - triggers hyperglycaemia
2 - triggers hypotension
3 - triggers catabolism
4 - triggers gluconeogenesis

A

3 - triggers catabolism

  • skeletal muscle is broken down
50
Q

Partial pressure is a measure of a single gas component in a mixture of gases. Partial pressure of oxygen in arterial blood (PaO2) is normally what?

1 - 50mmHg
2 - 70mmHg
3 - 90mmHg
4 - 100mmHg

A

4 - 100mmHg

  • <60mmHg signifies respiratory failure
  • Co2 is 45mmHg
51
Q

Partial pressure is a measure of a single gas component in a mixture of gases. Partial pressure of oxygen in arterial blood (PaO2) is normally 100mmHg. If this drops below 60mmHg this can cause respiratory failure. FiO2 is the concentration of O2 that is contained in the inspired air (FiO2). To calculate this we use the formula:

PaO2 (P)/ FiO2 (F)
Normal PaO2 = 100mgHg
Normal FiO2 in air is 21%
= 100 (P) / 0.21 (F) = 476 mmHg (kPa)

Which of the following would indicate severe acute respiratory syndrome which could be
suggestive of sepsis?

1 - < 100 mmHg (kPa)
2 - < 200 mmHg (kPa)
3 - < 300 mmHg (kPa)
4 - < 400 mmHg (kPa)

A

1 - < 100 mmHg (kPa)

  • normal is >400 mmHg (kPa)
52
Q

At a cellular level what happens to the mitochondria during septic shock?

1 - too much O2 reaching the mitochondria
2 - inability of O2 to diffuse into the matrix
3 - insufficient O2 delivered to mitochondria

A

3 - insufficient O2 delivered to mitochondria

53
Q

Which of the following produced by Staphylococcus aures is responsible for releasing toxins that can kill white blood cells and cause damage to skin and deeper areas such as muscle as in the image:

1 - Panton Valente Leucocidin
2 - Clostridium difficile
3 - Klebsiella oxytoca
4 - Clostridium perfringens

A

1 - Panton Valente Leucocidin

54
Q

Which of the following produced by Staphylococcus aures is responsible for releasing toxins that can cause severe epithelial and mucosal damage especially colonic mucosa?

1 - Panton Valente Leucocidin
2 - Clostridium difficile
3 - Klebsiella oxytoca
4 - Clostridium perfringens

A

4 - Clostridium perfringens

55
Q

Which of the following are not part of the Q-SOFA score that can help identify if a patient is at risk of organ dysfunction due to sepsis?

1 - low blood pressure (SBP≤100 mmHg)
2 - high respiratory rate (≥22 breaths per min)
3 - lactate >8mmol/L
4 - altered mentation (Glasgow coma scale<15).

A

3 - lactate >8mmol/L

56
Q

Antibiotics should be started within one hour of identifying someone with sepsis. How can we decide what antibiotics to prescribe a patient?

1 - use your own judgement
2 - speak to clinical supervisor
3 - look at research papers
4 - use trust guidelines

A

4 - use trust guidelines

57
Q

Patients with sepsis can develop Disseminated Intravascular Coagulation (DIC). What is DIC?

1 - body is unable to form blood clots
2 - blood clots form intravascular
3 - coagulation cascade is accentuated and uses up lots of platelets and clotting factors
4 - platelets are unable to function

A

3 - coagulation cascade is accentuated and uses up lots of platelets and clotting factors

  • if there are no platelet and coagulation factors left then patients can bleed very easily anywhere in the body
58
Q

Which 2 bacteria are common associated with toxic shock syndrome, a form of sepsis?

1 - mycobacterium tuberculosis
2 - staphylococcal
3 - streptococcal
4 - escherichia coli

A

2 - staphylococcal
3 - streptococcal

59
Q

Afterload is important in distributive shock. What is afterload?

1 - pressure required to fill the heart
2 - pressure required to fill atrium
3 - pressure heart has to pump against to pump blood out of the heart
4 - pressure required to return blood form the lungs to the heart

A

3 - pressure heart has to pump against to pump blood out of the heart

60
Q

What is obstructive shock?

1 - inability of heart to pump sufficient blood
2 - physical obstruction of blood
3 - physical blockage of the lungs
4 - loss of fluid and electrolytes

A

2 - physical obstruction of blood

C. Year 3: SBOM (50 decks)

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