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CCP S2 > CCP 226 - Immune > Flashcards

CCP 226 - Immune Flashcards

1
Q

What is INR dependent on?

A

Vitamin K factors 2, 7, 9, and 10.

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2
Q

What is the timeline of usefulness of INR?

A

INR is dependent partially on factor 7, which has the shortest half-life of the vitamin K factors, being 7 hours.

INR abnormality indicates liver malperfusion for at least 7 hours.

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3
Q

Poor end-organ perfusion of the lungs manifests as:

A

Leakiness, being ARDS.

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4
Q

What are the five types of MI?

A 
Type I - Occlusion
Type II - Demand 
Type III - Sudden death
Type IV - PCI
Type V - CABG
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5
Q

Each delay of 1hr in sepsis equates to an increased mortality of:

A

8%

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6
Q

List the four main components of sepsis management:

A
  1. Cultures and source control (ie. biliary blockage)
  2. Antibiotics
  3. Perfusion
  4. Adjuncts (ie. vasopressors, steroids, vitamin C, thiamine)
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7
Q

Gram negative bacteria are generally located:

A

Subdiaphragmatic.

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8
Q

PlasmaLyte contains more potassium than NaCl. Should NaCl be used in hyperkalemic septis patients?

A

No. PlasmaLyte is likely the better option because it has a higher pH than NaCl. The increase in pH will cause a more profound shift of K back into cells compared with the minute amount of K being added to serum by PlasmaLyte.

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9
Q

What is the sepsis MAP goal in early resuscitation?

A

MAP ≥ 65.

This can later be tailored to end-organ perfusion.

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10
Q

A higher MAP goal (ie. 80) may be beneficial in what septic populations?

A

Patients with CKD or chronic HTN.

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11
Q

Lactate clearance of ___%/hr indicates adequate end-organ perfusion.

A

20%/hr.

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12
Q

As norepinephrine doses rise, what adjunct should be considered?

A

Vasopressin.

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13
Q

Why is phenylephrine rarely used as an infusion?

A

Associated with the risk of digit ischemia.

Phenylephrine does have a role in pure SVR creation in patients with LVOT obstruction.

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14
Q

What are two pitfalls of epinephrine infusion?

A
  1. Causes rise in skeletal lactate production, which skews data trending.
  2. More arrhythmogenic than other pressors.
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15
Q

Is hydrocortisone a glucocorticoid, mineralocorticoid, or both?

A

Both.

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16
Q

What is the dose of hydrocortisone in sepsis, and what is it’s role in sepsis management?

A

50mg IV q6hr.

Useful in maintaining vasopressor effectiveness. Also assists in patients who have low ACTH (ie. low cortisol). No documented effect on mortality.

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17
Q

What is the role of thiamine and vitamin C in sepsis?

A

Both may assist the in effectiveness of the Kreb cycle. Both currently being investigated.

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18
Q

A CD4 count of __ is adequate in patients with HIV.

A

> 400.

An undetectable viral load is the goal of therapy in HIV.

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19
Q

List three common gram positive infections:

A
  1. MRSA.
  2. Strep.
  3. Staph.
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20
Q

List three common gram negative infections:

A
  1. SPACE bugs.
  2. Extended spectrum beta-lactamases (ESBLs)
  3. Carbapenamase-producing organism (CPOs)
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21
Q

What lab value is expected to be elevated in early infection?
HINT: WBC.

A

Band cells.

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22
Q

The PCADS mnemonic for the pillars of treatment of sepsis stands for:

A
  1. Perfusion
  2. Cultures
  3. Antibiotics
  4. Diagnose
  5. Source control
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23
Q

Patients who have been receiving steroid therapy with the last __ months prior to sepsis diagnosis should continue receiving steroid therapy.

A

2 months.

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24
Q

Epidermal and dermal infections are almost always gram ____.

A

Positive.

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25
Q

Necrotizing fasciitis affects what layer of skin.

A

The fascia.

Requires immediate debridement.

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26
Q

Myositis is the infection of ____.

A

Skeletal muscle.

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27
Q

Osteomyelitis is:

A

Infection of bone.

28
Q

Explain the pathophysiological process of fluid extravasation in sepsis:

A
  1. Microbe elicits an innate immune response
  2. Inflammatory response is produced by IL 1, 6, and TNF.
  3. Inflammation spreads the membrane-like wall of the vasculature, allowing for fluid to escape into the interstitium.
29
Q

Explain the pathophysiological process of mitochondrial dysfunction in sepsis:

A

Immune mediators produce mitochondrial dysfunction. The management of this is to support the body through illness, so it can eventually regain balance on it’s own.

30
Q

Explain the pathophysiological process of septic cardiomyopathy:

A

Cardiomyopathy is produced by inflammatory mediator disruption of myocyte activity. Causes troponin elevation, myocardial depression, and some ECG changes.

31
Q

Explain why DIC exists in sepsis:

A

Normally, vasodilation occurs from cGMP synthesis, which is facilitated by NO excreted by cells. DIC results when cGMP release comes to a halt once muscle stores of NO are exhausted (accompanied by vasoconstriction).

32
Q

What direction does hemoglobin g/L tend to move in sepsis?

A

Initially hemoglobin g/L will increase from extravasation of water. Later, Hgb will drop from fluid resuscitation.

33
Q

Mucous membrane hydration is dependent on ___ compartment.

A

The interstitial fluid compartment.

34
Q

What role does vitamin C play in the management of sepsis?

A

1) May enhance mitochondrial health.

2) Assists anticoagulation in the setting of DIC.

35
Q

What role does IV nitroglycerin have in the management of sepsis?

A

Provides NO that can be used to vasodilate in late sepsis when the tissues are exhausted of NO.

36
Q

What role does heparin have in the management of sepsis?

A

Heparin may reduce coagulation in the setting of DIC.

37
Q

SIRS Criteria:

A

1) Temp > 38 or < 36
2) HR > 90
3) RR > 20 or PaCO2 <32
4) WBC > 12000 or < 4000, or > 10% band cells (granulocytes, think “grandkids”)

38
Q

Explain the physiology of thirst:

A

Osmoreceptors in the brain detect increased tonicity within themselves. They then stimulate the hypothalamus to make the body sense thirst. The hypothalamus then stimulates the pituitary to release ADH, which causes vasoconstriction and H2O retention in the nephron.

High osmolality produces thirst, with NO differentiation between high solutes vs low total body water.

39
Q

Septic is latin for the word:

A

Rotten.

40
Q

Explain the pathophysiology of sepsis:

A
  1. WBC gather to fight infection & recruit inflammatory mediators.
  2. WBCs release NO, causing leakiness of the vessels and vasodilation. This response becomes systemic.
  3. Cells become hypoxic from abundance of interstitial fluid between vessel/membrane impairing oxygen diffusion.
  4. Blood vessels are damaged by lytic cells and enzymes. Produces DIC.
  5. ARDS may develop from microvascular damage associated with DIC.
  6. Cardiac output initially increases, but falls eventually when septic cardiomyopathy begins from inflammatory mediators, acidosis, and ischemic from DIC.
  7. Vasoconstriction begins in late stages from exhausted of NO stores in muscle. The permeability of vessels continues because of damage imposed on vessels from lytic enzymes.
41
Q

What is the initial recommended fluid bolus in sepsis?

A

30mL/kg initial bolus.

42
Q

How is a passive leg raise performed?

A

Elevate the legs to 45 degrees for 40-60 seconds, looking for increase in ABP MAP or decrease in HR.

43
Q

pH increases by ___ for every 10 mmHg decrease in PaCO2 below 40.

A

0.08.

44
Q

pH decreases by ___ for every 10 mmHg increase in PaCO2 above 40.

A

0.08.

45
Q

Pulse pressure variation is indicative of:

A

Fluid depletion.

46
Q

Consider a CVP of 6, that is unchanged by a 1L bolus of fluid; What might this indicate?

A

Fluid depletion.

47
Q

IVC collapsibility on inspiration in a spontaneous breathing patient indicates ___.

A

Fluid depletion.

48
Q

The oxygen delivery equation is ___.

A

DO2 = CO x ([1.34 x Hgb x SaO2] / [0.0031 x PaO2])

49
Q

The oxygen consumption equation is ____.

A

VO2 = CO x (CaO2 - CvO2)

50
Q

Normal VO2 in a conscious & resting person is ___mL O2/min.

A

250mL O2/min.

51
Q

The oxygen extraction ratio is calculated using:

A

O2ER = (CaO2 - CvO2) / CaO2

52
Q

What is a normal oxygen extraction ratio?

A

0.25 - 0.3

53
Q

Normal calcium levels are:

A 
Ionized = 1.1
Total = 2.1
54
Q

For every 10 decrease in albumin, you have a decrease of ___ total calcium.

A

0.2

55
Q

Normally calcium and hydrogen compete for binding of proteins. Why do we often see hypocalcemia in septicaemia?

A

Sepsis reduces the secretion of PTH. The requirement to maintain endothelial constriction and myocardial contraction also depletes ionized calcium stores.

56
Q

What steroid is the TOC in septic patients with adrenal insufficiency?

A

Hydrocortisone 50-100mg q6hr.

57
Q

What produces refractory vasodilatory shock in sepsis?

A

cGMP can produce refractory vasodilation. Methylene blue is the TOC as it scavenges excess cGMP.

58
Q

What are two uses of methylene blue?

A

1) Refractory vasodilatory shock from excess cGMP.

2) Methylhemoglobinemia.

59
Q

What is the “delta down”?

A

The difference between systolic blood pressure with pulse pressure variation during respiration.

60
Q

What is the “big kahuna” antibiotic for treatment of gram negative bugs?

A

Merepenum.

Merepenum deletes all of the SPACE bugs.

61
Q

What are bacteriacidal antibiotics?

A

Antibiotics that function by killing bacteria, by either:

a) Cell wall destruction.
b) Cell membrane destruction.

62
Q

What are bacteriostatic antibiotics?

A

Antibiotics that slow the replication of bacteria via:

a) RNA/DNA interruption.
b) Inhibition of protein synthesis at the ribosome.
c) Inhibition of folic acid production.

63
Q

What is the VAP prevention bundle?

A 
H - HOB up
O - Oral care 
S - Sub/supra glottic suctioning (hourly)
E - Extubation
S - Safe ICU nutrition
64
Q

Explain the pathogenesis of VAP:

A

1) Microaspiration of URT and GI aspirations (80%)

2) Biofilm colonization. This is why we don’t routinely flush the ETT when suctioning.

65
Q

What is the berlin criteria?

A

1) PF ratio < 300
2) Bilateral opacities on CXR not fully explained by effusions, lung collapse, or nodules.
3) Respiratory failure not fully explained by cardiac failure.
4) Pulmonary insult within 1 week.

66
Q

List the sepsis continuum:

A

I) SIRS
II) Sepsis
III) Septic shock
IV) MODS

67
Q

List the components of the “within 1 hr” sepsis bundle:

A

1) Measure lactate
2) Obtain cultures
3) Begin broad-spectrum ABx
4) Isotonic 30mL/kg bolus if MAP < 65 or Lactate > 4
5) Vasopressor if MAP < 65 (following fluid admin)

CCP S2 (10 decks)

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