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HDM Final > SIRS CIS > Flashcards

SIRS CIS Flashcards

1
Q

What does SIRS stand for?

A

Systemic Inflammatory Response Syndrome

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2
Q

SIRS results from pathogenic over-stimulation of the immune response. If the pathogen is non-infectious in origin, what is the end result?

A

Shock

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3
Q

SIRS results from pathogenic over-stimulation of the immune response. If the pathogen is infectious in origin, what is the end result?

A

Sepsis and septic shock

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4
Q

Are the majority of cases of SIRS leading to shock infectious or non-infectious in origin?

A

Non-infectious

[infectious only accounts for about 43% of SIRS leading to shock]

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5
Q

When might you see an uptick in the percentage of septic shock cases?

A

Septic shock cases are infectious in origin, would see during epidemics of pathogens containing superantigens

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6
Q

Pancreatitis, trauma, burns, etc. are associated with what type of SIRS?

A

Non-infectious

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7
Q

When do symptoms appear during the phased inflammatory response exhibited by SIRS patients?

A

Symptoms appear during hyperinflammatory phase

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8
Q

What is the patient’s immune response called when they first respond to the hyperinflammatory phase of SIRS?

A

Compensatory anti-inflammatory response (CARS)

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9
Q

T/F: during the CARS period of a SIRS response, the patient is significantly immunosuppressed

A

True

The immune system will continue to rebound with hyperinflammatory reactions, leading to another compensatory response, each one becoming less severe until homeostasis is reached

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10
Q

At least 2 of a set of criteria are needed to make the SIRS diagnosis. What are the 4 criteria?

A

Body temp (above 38 or below 36)

Heart rate (greater than 90 bpm)

Respirations (greater than 20/min or PaCO2 less than 32 mm Hg)

WBC count (greater than 12x10^9/L or less than 4x10^9/L)

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11
Q

What criteria is needed for SIRS to be considered sepsis?

A

SIRS + infection

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12
Q

What criteria is needed for the diagnosis of SEVERE sepsis?

A

Sepsis associated with organ dysfunction, systemic hypoperfusion, or hypotension

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13
Q

What criteria is needed for the diagnosis of septic shock?

A

Sepsis with arterial hypotension despite adequate fluid replacement

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14
Q

What are some examples of initial insults to the system that may lead to SIRS?

A 
Uncontrolled infection
Major trauma
Circulatory shock
Tissue necrosis
Apoptosis
Anaphylaxis
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15
Q

Initial systemic insult is followed by a trigger in order to propagate toward a SIRS response. What are these triggers?

A

PAMPs or DAMPs

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16
Q

Which of the following is not a PAMP?

A. Lipopolysaccharide
B. Peptidoglycan
C. Uric acid
D. Lipotechoic acid

A

C. Uric acid

[uric acid, HMGB-1, heat-shock protein, and DNA are DAMPs]

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17
Q

What are the 3 categories of sensors and effector cells that respond to PAMPs and DAMPs that lead to SIRS?

A

Complex protein systems (complement, coagulation)

Vascular and tissue cells (endothelium, epithelium, adipose)

Blood and lymphatic cells (granulocytes, macrophages/monocytes, lymphocytes)

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18
Q

When SIRS impacts organ function, what effect might it have on the brain?

A

Confusion

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19
Q

When SIRS impacts organ function, what effect might it have on the lungs?

A

Respiratory distress

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20
Q

When SIRS impacts organ function, what effect might it have on the cardiovascular system?

A

Shock

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21
Q

When SIRS impacts organ function, what effect might it have on the kidney?

A

Oliguria/anuria

[severely diminished urine output]

22
Q

When SIRS impacts organ function, what effect might it have on the liver?

A

Excretory failure

23
Q

When SIRS impacts organ function, what effect might it have on the gut?

A

Loss of barrier function, ileus

[ileus = inability of the bowel to contract normally and move waste out of the body]

24
Q

When SIRS impacts organ function, what effect might it have on microcirculation?

A

Capillary leak, edema, DIC

25
Q

The ___________ is a signaling system for the detection of pathogens and stressors. It involves the assembly of a sensor (NLRP3) and adaptor (ASC) and an inactive caspase (caspase-1).

A

Inflammasome

26
Q

What is the sensor involved in formation of the inflammasome?

A

NLRP-3

27
Q

What does the inflammasome do with the inactive caspase, and what cytokines does it produce?

A

Activates the caspase, which in turn results in the expression of IL-1

Eventually results in production of both IL-1 and IL-18, which are potent inflammatory cytokines

28
Q

How does the inflammasome contribute to the production of IL-1? (Specifically)

A

Innate immune signals coming from things like TLR stimulation in the nucleus result in transcription of Pro-IL-1-beta

The inflammasome produces active caspase-1, which acts on Pro-IL-1-beta to make it IL-1-beta which can then be secreted and cause acute inflammation

29
Q

What are the innate acute phase cytokines that contribute to SIRS and Shock, and in what order are they produced?

A

TNF –> IL-1 –> IL-6

30
Q

What anaphylotoxin is produced prior to the acute phase cytokines in SIRS and shock?

A

C5a

31
Q

The innate acute phase cytokines stimulate the liver to produce what?

A

Yet more acute phase proteins, including CRP and C’

32
Q

What does DIC stand for?

A

Disseminated intravascular coagulation

[responsible for inadequate blood flow and tissue perfusion]

33
Q

What tissues are most susceptible to DIC?

A

Lungs, liver, and kidneys because they are highly vascularized with very small vessels

34
Q

What complication of SIRS results in diffuse cerebral dysfunction caused by a systemic inflammatory response, and is the most frequent cause of delirium in critical illness due to tissue hypo-perfusion?

A

Sepsis Associated Encephalopathy

35
Q

T/F: The MAJORITY of patients with severe systemic infections will experience fluctuating mental status changes, inattention, disorganized thinking, and loss of consciousness

A

True, about 70% of patients with severe systemic infections will experience these symptoms

36
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome

Results from vasodilation and edema in alveolar spaces followed by recruitment of phagocytes and deposition of microthrombi and fibrin

37
Q

What is the two-hit theory associated with SIRS?

A

There is an initiating event followed by some recovery, then a second hit results in worsened condition

38
Q

What are some of the “first hits” associated with SIRS?

A

Injury
Hypotension
Hypoxia

39
Q

What are some examples of “second-hits” associated with SIRS?

A

Often iatrogenic in nature
Reperfusion of ischemic areas
Antimicrobial agents
Surgical procedures

40
Q

What is the Jarisch-Herxheimer reaction?

A

Occurs when someone in a state of shock is given antibiotics for the pathogen which causes lysis and release of more PAMPs, resulting in temporary symptom relief followed by a worsened state of shock

41
Q

Cellular and molecular elements of the CARS response include:

Lymphocyte dysfunction and _____________

Downregulation of _____/co-stimulatory receptors

________ deactivation

Cytokine production including _____ and ______

A

Apoptosis

HLA

Macrophage

IL-10; TGF-beta

42
Q

What are some of the clinical elements of the CARS response?

A 
Cutaneous anergy
Hypothermia
Leukopenia
Susceptibility to infection
Failure to clear infection
43
Q

Shock may lead to immune exhaustion, what does this mean?

A

Depletion of mediators like cells and serum proteins leads to immunosuppressive state

Low expression of HLA class I and B7, poor APC function

Myeloid derived suppressor cells and IL-10

44
Q

Are investigational strategies like anti-TNF polyclonal antibodies and activated protein C effective in the treatment of shock?

A

No, they were found to disrupt the physiological balance of cytokines and led to increased mortality risk

45
Q

What is the only treatment that has found to be effective for SIRS?

A

Cytosorb, a hemodialysis filter that is able to filter out acute phase cytokines

46
Q

Does IVIG work for SIRS or sepsis?

A

Only for sepsis

47
Q

What is the most common clinical presentation of pneumonia among adults?

A

Pneumococcal pneumonia

48
Q

What is the incubation period for pneumococcal pneumonia?

A

1-3 days - very short, become sick very quickly

49
Q

Why is streptococcus pneumonia often considered to be “community-acquired”?

A

Because the majority of the population are carriers

50
Q

How does the clinical presentation of streptococcus pneumoniae differ in children vs. adults?

A

Causes pneumococcal meningitis in children

Causes pneumonia in adults

51
Q

What are some issues that affect SIRS patients after recovery?

A

Although there is a decreasing death rate for SIRS in the US, there is an increased risk of death in the year following recovery. There is also impaired physical and neurocognitive function, leading to an overall lower quality of life.

HDM Final (12 decks)

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