Sepsis and Septic Shock

Question 1

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

Answer 1

3 - infection causing widespread and systemic inflammation

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

Question 2

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

Answer 2

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

Question 3

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

Answer 3

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

Question 4

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%

Answer 4

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

Question 5

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

Answer 5

4 - 40-70,000

Question 6

What is the leading cause of ICU death?

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

Answer 6

2 - sepsis

Question 7

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

Answer 7

1 - PRRs binding to antigens of microbials

• pattern recognition receptors identify foreign pathogens

Question 8

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

Answer 8

4 - neutrophils and macrophages

Question 9

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

Answer 9

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

Question 10

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

Answer 10

3 - factor XII

Question 11

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

Answer 11

4 - become damaged and leaky

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

Question 12

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

Answer 12

1 - cytokines loosen tight junctions

Question 13

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

Answer 13

4 - cause vasodilation and reduced BP

• main cause of hypotension in sepsis patients

Question 14

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

Answer 14

1 - fever, coagulopathy, vasodilation, capillary leaking

• fever = cytokines signal to hypothalamus to increase body temperature
• inflammation initiates coagulation cascade
• nitric oxide and cytokines induce vasodilation
• capillary leaking is due to relaxed/damaged tight junctions and increased fluid

Question 15

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

Answer 15

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

Question 16

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?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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)

Answer 19

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

Question 20

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)

Answer 20

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

Question 21

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)

Answer 21

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

• giving fluid will not help with this

Question 22

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

Answer 22

3 - atrial natriuretic peptide

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

3 - anaerobic glycolysis and excessive lactate production

• high lactate causes metabolic lactic acidosis

Question 25

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

Answer 25

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

Question 26

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

Question 27

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

Answer 27

2 - increased insulin resistance and increases blood glucose

Question 28

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

Answer 28

2 - increased insulin resistance and increases blood glucose

• insulin release is impaired
• GLUT 4 is impaired

Question 29

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

Answer 29

4 - T3 and T4

• thyroid hormone release would have the opposite effect

Question 30

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

Answer 30

3 - adrenal gland necrosis

• glucocorticoid levels drop

Question 31

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

Answer 31

7 - anaphylaxis

Question 32

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

Answer 32

2 - increase of >2 point

Question 33

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

Answer 33

3 - hypotension with MAP <65mmHg

• even with the use of vasopressors (increase BP)

Question 34

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

Answer 34

1 - serum lactate >2mmol despite fluid resuscitation

Question 35

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

Answer 35

1 - tachypnea

Question 36

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

Answer 36

3 - deviated trachea

Question 37

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

Answer 37

Additional fluid in the lungs is due to leaking capillaires

Question 38

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

Answer 38

3 - bind non-specifically to any T cells

Question 39

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

Answer 39

1 - leads to overactive immune response

• huge inflammatory response follows due to cytokine release
• means that T cells are unable to bind to the antigen on the pathogen

Question 40

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

Answer 40

2 - produced protein toxins that bind inactivate antibodies

• cause toxic shock syndrome

Question 41

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%

Answer 41

3 - 50%

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

Question 42

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

Answer 42

1 - toll like receptors

• specifically toll-like receptor 2 (TLR2)

Question 43

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

Answer 43

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

Question 44

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

Answer 44

3 - toxic shock syndrome

Question 45

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

Answer 45

5 - Recent course of antibiotics

Question 46

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

Answer 46

4 - monitor ECG

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

Question 47

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

Answer 47

3 - distributive

Question 48

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

Answer 48

4 - Lactate >2mmol/L

Question 49

Why can sepsis lead to cachexia?

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

Answer 49

3 - triggers catabolism

• skeletal muscle is broken down

Question 50

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

Answer 50

4 - 100mmHg

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

Question 51

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)

Answer 51

1 - < 100 mmHg (kPa)

• normal is >400 mmHg (kPa)

Question 52

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

Answer 52

3 - insufficient O2 delivered to mitochondria

Question 53

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

Answer 53

1 - Panton Valente Leucocidin

Question 54

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

Answer 54

4 - Clostridium perfringens

Question 55

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).

Answer 55

3 - lactate >8mmol/L

Question 56

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

Answer 56

4 - use trust guidelines

Question 57

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

Answer 57

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

Question 58

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

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

Answer 58

2 - staphylococcal
3 - streptococcal

Question 59

Afterload is important in distributive shock. What is afterload?

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

Answer 59

3 - pressure required to pump blood out of the heart

Question 60

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

Answer 60

2 - physical obstruction of blood