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Micro > 02a: Sepsis > Flashcards

02a: Sepsis Flashcards

1
Q

2016 definition of sepsis:

A

Life-threatening organ dysfunction caused by a dysregulated host
response to infection

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2
Q

Diagnosis of SIRS requires 2 out of which 4 criteria?

A
  1. Body T (under 35C or over 39C)
  2. HR over 90 bpm
  3. RR over 20 breaths/min, aCO2 under 32 mmHg, or required mechanical ventilation
  4. WBC over 12,000, under 4000, or over 10% bandemia
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3
Q

Difference between sepsis and SIRS.

A

Sepsis is SIRS due to an infectious etiology

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4
Q

T/F: The total number of cases of sepsis and the number of patients who are dying is increasing.

A

True

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5
Q

T/F: Causes of SIRS are nearly always infectious agents.

A

False - could be infectious, trauma, pancreatitis, etc.

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6
Q

T/F: For SIRS resulting from sepsis, Gram-pos infections more frequent than Gram-neg.

A

True

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7
Q

A simple definition of (X) is “blood outside the blood vessel”. List the types of (X).

A

X = hemorrhage;

  1. Hematoma
  2. Petechiae
  3. Purpura
  4. Ecchymoses
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8
Q

(X) is the medical term for “bruise”, which is typically 1-2 (mm/cm/in).

A

X = ecchymoses

1-2 cm

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9
Q

Patients with low platelet counts develop which type of hemorrhages? They’re typically 1-2 (mm/cm/in).

A

Petechiae (small);

1-2 mm

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10
Q

List the steps of normal hemostasis.

A
  1. Arteriolar vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Anti-thrombotic events
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11
Q

In (primary/secondary) hemostasis, (X) factor serves as bridge between ECM proteins and platelets.

A

Primary;

X = von Willebrand’s

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12
Q

In secondary hemostasis, (X) needs to be stabilized through activation of (Y).

A 
X = platelet plug
Y = coagulation cascade (results in local fibrin deposition)
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13
Q

Plasminogen activaor inhibitors are (pro/anti)-coagulant.

A

Pro-coagulant

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14
Q

Thrombin is (pro/anti)-coagulant and functions to:

A

Pro-coagulant;

Cleaves fibrinogen

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15
Q

Tissue factor is (pro/anti)-coagulant and functions to:

A

Pro-coagulant;

Activates extrinsic clotting cascade

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16
Q

T/F: Under normal circumstances, endothelial cells have strong pro-thrombotic properties.

A

False - anti-thrombotic (quickly change to pro-thrombotic state upon injury)

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17
Q

Describe the anti-platelet effect of vascular wall endothelial cells.

A
  1. Physical barrier between platelet and ECM proteins)

2. Secrete prostacyclin, NO (vasodilation and inhibit platelet aggregation)

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18
Q

Describe the anti-coagulant effect of vascular wall endothelial cells.

A

Membrane has:

  1. Heparin-like molecules
  2. Thrombomodulin
  3. Tissue factor pathway inhibitor
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19
Q

Describe the fibrinolytic effect of vascular wall endothelial cells.

A

Cells produce tissue type plasminogen activator (tPA), enhancing breakdown of fibrin

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20
Q

Which pro-thrombotic factors are produced by vascular endothelial cells?

A
  1. Von Willebrand factor
  2. Tissue factor
  3. Plasminogen activator inhibitors (PAIs)
21
Q

Protein C and S are (pro/anti)-coagulant and function to:

A

Anti-coagulant;

Inhibit clotting factors

22
Q

Thrombomodulin is (pro/anti)-coagulant and functions to:

A

Anti-coagulant;

Binds thrombin and activates protein C

23
Q

Normally, platelets circulate freely in the blood. When exposed to (X), which 3 reactions favor thrombus formation?

A

X = ECM proteins

  1. Adhesion
  2. Secretion
  3. Aggregation
24
Q

A genetic deficiency in vWF (von Willebrand factor) may result in (hypercoagulation/excessive bleeding).

A

Excessive bleeding;

vWF serves as bridge between platelet and ECM collagen during thrombus formation

25
Q

Thrombus formation: once platelets have adhered to ECM, (X) step occurs. Which two factors are important here?

A

X = secretion (of granule contents)

  1. Ca (activates coagulation cascade)
  2. ADP (aggregates platelets)
26
Q

Heparin injected by doctors into patients is used for (pro/anti)-coagulation purposes. What’s the mechanism?

A

Anti-coagulation;

Binds and activates anti-thrombin

27
Q

Molecule that interferes with fibrin polymerization and breaks down fibrin.

A

Plasmin

28
Q

List the three factors that contribute to thrombus formation. Star the most crucial of these.

A
  1. Endothelial cell damage*
  2. Hypercoagulable state
  3. Abnormal blood flow (i.e. turbulent, slow)
29
Q

Primary hypercoagulability state are due to

X

A

X = genetic alterations (mutations/deficiencies of coagulation pathway elements)

30
Q

Secondary

hypercoagulability state is called this because:

A

It is secondary to another disease state or clinical condition.

31
Q

T/F: Primary hypercoagulability more common than secondary hypercoagulability.

A

False - vice versa

32
Q

Arterial thrombi arise at site of (X) and venous thrombi at site of (Y).

A 
X = injury (ex: atherosclerosis)
Y = stasis
33
Q

(Arterial/venous) thrombus has lines of Zahn and is (more/less) firmly attached than (arterial/venous) thrombus.

A

Arterial;
More;
Venous

34
Q

List the fate of thrombus (if patient survives).

A

Acronym PEDO

  1. Propagate (grow/occlude)
  2. Embolize (freed/travels)
  3. Dissolution (fibrinolysis lyses it)
  4. Organize/recanalize (fibrosis with new vascular channels)
35
Q

Disseminated intravascular coagulation (DIC) is clinical condition in which:

A

There is widespread formation of numerous fibrin thrombi throughout the micro-vasculature

36
Q

A detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin.

A

Embolus

37
Q

Pulmonary thromboemboli are formed from:

A

Deep veins of pelvis/legs

38
Q

After long bone fractures, (X) emboli may form.

A

X = fat

39
Q

(X) embolism may form secondary to changes in atmospheric pressure. This is called (Y) sickness.

A 
X = air 
Y = decompression
40
Q

Following tear in amniotic membrane, (X) an embolus, composed of (Y) cells, can be found in which location in (fetus/mother)?

A 
X = amniotic fluid 
Y = squamous cells (from fetal skin)

Maternal pulmonary microcirculation

41
Q

(X) emboli are caused by pieces of necrotic, infected tissue.

A

X = septic

42
Q

(X) is an area of ischemic necrosis secondary to occlusion of the vasculature.

A

X = infarct

43
Q

White, aka (X), infarcts occur in which situation(s)?

A

X = anemic

(End) arterial occlusion

44
Q

(X) is the clinical state of systemic hypoperfusion.

A

X = Shock

45
Q

List the five types of clinical “shock”.

A
  1. Cardiogenic
  2. Septic
  3. Hypovolemic
  4. Anaphylactic
  5. Neurogenic
46
Q

Septic patients have (excess/delayed) neutrophil

apoptosis.

A

Delayed (cells persist longer in bloodstream)

47
Q

Septic patients have (excess/delayed) lymphocyte

apoptosis.

A

Excess/accelerated

48
Q

Sepsis mortality can be predicted quickly via SOA (sequential organ failure assessment). Which factors are considered here? How accurate is this screen?

A
  1. RR over 20/min
  2. Altered mentation
  3. Systolic BP under 100 mmHg

Accurately screens 2/3

Micro (16 decks)

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