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Perf Tech II (exam 1) > Topic 2 > Flashcards

Topic 2 Flashcards

1
Q

circulating mast cells called?

A

Basophils

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2
Q

Heparin structure

A

Sulfated glycosaminoglycan present in mast

cells

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3
Q

Heparan

A

close relative to heparin

lower sulfated form present on endothelial cells

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4
Q

Heparin works predominantly via potentiation of …

A

potentiation of Antithrombin III (AT III) to neutralize circulating thrombin and other activated serine proteases (VII, IX, X, XI, XII)

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5
Q

Unfractionated Heparin

A

most commonly used type of heparin by perfusionists (because it is cheaper)

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6
Q

Long chains of unfractionated Heparin

A

(higher MW) bind better with AT-III and thrombin

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7
Q

In unfractionated Heparin_____ required for AT-III interaction

A

Specific pentasaccharide sequence along heparin chain

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8
Q

Unfractionated Heparin molecular weights

A

Range 3,000 - 40,000+ Daltons

Distribution of MW varies depending on source

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9
Q

Highest negative charge density of any biological molecule

A

Heparin (very! acidic)

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10
Q

Heparin Predominantly works via potentiation of Antithrombin III (AT III) to neutralize circulating thrombin and and other
activated serine proteases which are?

A

Activated serine proteases (VII, IX, X, XI, XII)

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11
Q

Mucosal Heparin MW

A

lower than Lung Heparin

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12
Q

Lung Heparin potency

A

greater potency than mucosal heparin so need a lower dose

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13
Q

Heparin more likely to cause HIT ?

A

Lung Heparin

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14
Q

Why does Lung Heparin need a larger protamine dose compared to Mucosal Heparin?

A

Lung Heparin requires more protamine due to having more ATIII interactions than Mucosal Heparin

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15
Q

Mucosal Heparin protamine dose needed compared to Lung Heparin

A

Need 25-30% less Protamine to neutralize

Lower MW which uses Xa inhibition– not reversed by Protamine

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16
Q

1 United States Pharmacopoeia (USP) unit

A

amount of heparin that maintains fluidity
of 1mL of citrated sheep plasma for 1 hour after
recalcification

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17
Q

British Pharmacopoeia (BP) units

A

Sulfated ox blood activated with thromboplastin

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18
Q

European Pharmacopoeia (EU) units

A

Recalcified sheep plasma in the presence of kaolin and cephalin incubated for 2 minutes therefore constituting an aPTT for sheep plasma

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19
Q

Heparin half life with 100U/kg dose = __ min

A

61 ± 9minutes

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20
Q

Heparin half life with 200U/kg dose = __ min

A

93± 6 minutes

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21
Q

Heparin half life with 400U/kg dose = __ min

A

126 ± 24 minutes

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22
Q

Heparin pharmacokinetics
_______ elimination with peak effects at __ minutes post administration via central line
—Delayed in states of ___ or with peripheral injection

A

Biphasic
1-2

low CO

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23
Q

Heparin pharmacokinetics

Redistribution after ____ to normal elimination

A

4 - 5 min

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24
Q

Hypothermia effect on Heparin

A

delays clearance and increases half-life

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25
Q

Heparin at 25*C

A

virtually constant for 40-100 min

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26
Q

Celsius to Fahrenheit

A

[°F] = [°C] × 9 / 5 + 32

short cut way (not totally accurate)
F = (C x 2) + 30

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27
Q

Fahrenheit to Celsius

A

[C] = [F] - 32 x 5 / 9

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28
Q

AT III in the presence of Heparin

A

is increased 1,000-10,000X

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29
Q

Size Chains of heparin that bind to AT III?

A

Only larger chain molecules (1/3) of heparin

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30
Q

Smaller Heparin chains primarily have ___ effect?

A

anti-Xa effect and minimal anti-IIa effects

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31
Q

In regards to the Initial Heparin dose:

  - What is the loading does?
  - What is the dose added to prime?
A
  • Loading dose of 200-400U/kg given

- 5,000 to 20,000U added to prime

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32
Q

Heparin Empiric dosing amount?

The loading dose is given now what additional heparin amount do you give?

A

Loading dose given and ACT verified.
After that, give additional heparin (50 to 100U/kg) every 30 minutes or as infrequently as every 2 hours.

(No ACT checked due to theory of existing variables that make ACT
inaccurate)

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33
Q

Young et al (1978) found fibrin formation when ACT dropped _____
(study involving 9 rhesus monkeys)

A

below 400 seconds

Recommended minimum value of 480 seconds do to 10% interspecies variation and 10% test variability

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34
Q

Gravlee Heparin Protocol STEPS (6)

A

**Prime ECC with 3U of heparin per milliliter of pump prime
**Initial dose 300U/kg IV
**Draw sample for ACT 2 to 5 minutes after infusion
**Give additional heparin as needed to achieve ACT above 400 seconds
before initiation of bypass
Give additional heparin as needed to maintain ACT above 400 seconds
during normothermic bypass
**Give additional heparin as needed to maintain ACT above 480 seconds
during hypothermic bypass (24 to 30C)
**Monitor ACT every 30 minutes during bypass or more frequently if patient
shows heparin resistance

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35
Q

Heparin Complications

A
  • *Heparin binds to platelets
  • *Insufficient heparinization on bypass causes consumption of clotting factors.
  • *Bleeding
36
Q

Heparin binding to platelets causes

A
  • Transient decrease in platelet count

- Prolonged bleeding time

37
Q

Heparin binding to platelets decreases with what?

A

Binding decreases with decreased MW (i.e.. LMWH)

38
Q

Heparin binding site to platelets

A

No specific binding site yet determined

39
Q

Heparin Resistance

A

When more than 600u/kg given and ACT still is <300 seconds

Higher than normal heparin doses for sufficient anticoagulation for bypass

40
Q

Extreme thrombocytosis

A

Platelet count > 500,000

41
Q

ATIII Deficiency causes?

A

Familial/ Congenital

Acquired (Due to continued heparin therapy or estrogen based contraceptives)

42
Q

Nitroglycerin

A

rare

Clinically relevant only when > 300 mcg/min

43
Q

Heparin Resistance causes (5)

A 
Extreme thrombocytosis
Septicemia
Hypereosinophilic Syndrome (rare)
Nitroglycerin (rare)
ATIII Deficiency
44
Q

ATIII Deficiency Inherited (Familial/Congenital)

Factors precipitating occurrence: (3)

A
  1. Pregnancy
  2. Infection
  3. Surgery
    Thrombosis after surgery
    Inability to get adequate anticoagulation for cardiac surgery
45
Q

ATIII Deficiency Inherited (Familial/Congenital) affects __ people?

A

1/2000 to 20,000 people

46
Q

ATIII Deficiency Inherited (Familial/Congenital)

Presents at what age range? and with what physical expression?

A

Presents @ 15-30 years old with low limb venous thrombosis or Pulmonary Embolism

47
Q

ATIII Deficiency Inherited (Familial/Congenital)

Gene expression?

A

Autosomal dominant

48
Q

ATIII Deficiency Inherited (Familial/Congenital) :

Treatment ?

A

Life long antithrombotic therapy after diagnosis

Decreases incidence of thromboembolic events by 65%

49
Q

Infants and newborns have __ levels of ATIII

A

60-80% adult ATIII levels

they dont have problems because Newborns don’t have thrombotic activity like adults do

50
Q

@ 3 months ATIII Levels

A

90% of adult levels

51
Q

Acquired ATIII Deficiency occurs how?

A

Occurs when patients are on Heparin pre-op or have chronic DIC
ATIII levels plateau around 60% of normal

52
Q

Acquired ATIII Deficiency treatment: (2)

A

Transfusion of FFP

Administration of Recombinant ATIII (Thrombate or ATryn)

53
Q

Platelet dysfunction can lead to

A

HIT

54
Q

Heparin (Lrg MW) readily binds to platelets inducing release of : (4)

A

PF4
activation of GPIIb/IIIa receptors
platelet degranulation
platelet aggregation

55
Q

HIT - Clinical condition characterized by a drop in platelet counts to ____ or _____from baseline

A

drop in platelet counts to <100,000 or 50% reduction from baseline

56
Q

HIT - typically seen in ?

A

5-28% of patients receiving heparin

2-10 days after initiation of heparin therapy (can w/in hours)

57
Q

HIT is less common with what types of Heparin?

A

LMWH and porcine mucosal heparin

58
Q

HIT Type 1 — appears when?

—platelet count normalizes when?

A
  • not immune mediated
  • appears withing first two days of heparin exposure (LMWH/unfractionated)
  • platelet count normalizes with continues heparin therapy

NOT Clinically significant

59
Q

HIT Type II - appears when?

- resolves?

A
  • immune mediated
  • appears 4-14 days after heparin exposure (mostly unfractionated)
  • can be life threatening
  • does not spontaneously resolve with continued heparin therapy
60
Q

HIT syndrom and HIT antibody have what correlation?

A

have a 90% correlation

Hit antibody causes HIT (but antibody presence alone does not mean they will get HIT!)

61
Q

ELISA assay

A

measures IGG antibodies to heparin/PF4 complexes

Sensitivity >90% (low specificity - many false positives)

62
Q

4 HIT antibody diagnostic test

A

1) ELISA assay
2) HIPA
3) C-SRA
4) PaGIA

63
Q

HIPA (Heparin-Induced Platelet Aggregation Assay)

A

Measures presence of antibodies to heparin/PF4 coplexes

High specificity/ ~50% sensitivity

64
Q

C-SRA (serotonin Release Assay)

A
  • measures serotonin released by platelets activated by the HIT antibodies
  • Sensitivity ~90% / Specificity ~100%
  • GOLD STANDARD
  • slow turn around/expensive/complex
65
Q

PaGIA (Particle Gel Immunoassay)

A

Uses polystryrene particles coated with PF4-heparin complexes, patient serum added and compared to a standard

  • quick and easy
  • high specificity, but lots of false positives
66
Q

How do you diagnosis HIT

A
  • Clinical Diagnosis
  • Thrombocytopenia (absolute or relative drop from baseline)
  • THROMBOSIS
  • Timing
  • Greinacher Scoring System
67
Q

HIT Risk Factores

A
  • Race (African Americans more likely)
  • Sex (females more likely)
    - does not occur in pregnant women
  • post organ transplant (very prone)
  • cardiac and orthopedic(more) patients prone
68
Q

% of HIT syndrome patients that are cardiac surgery patients

A

50%!

69
Q

% of HIT national prevalence in all heparin esposures

A

~0.2%

Includes quick procedures

70
Q

% of HIT patients that require limb amputation

A

~11%

71
Q

% HIT patients that die

A

25-30%

72
Q

HIT Anticoagulation treatments (3):

A
  • DTIs (Direct Thrombin Inhibitors)
  • Factor Xa inhibitors
  • Heparinoids

NEVER WARFARIN (if they did get warfarin give vitamin K)

73
Q

Lepirudin (Refludan)

  • what?
  • T1/2
  • Measured by?
  • given?
A

HIT, DTI anticoagulation treatment

  • recombinant leech-saliva anticoagulant
  • T1/2 ~80 minutes (up to 48hrs with renal dysfunction)
  • Measures by aPTT or ECT(eccrine clotting times)
  • Given SubQ or IV
  • Fairly immunogenic (allergic reaction)
74
Q

Bivalirudin (Angiomax)

  • what?
  • T1/2
  • immunogenic?
  • Measured/monitored by?
  • given?
A

HIT, DTI anticoagulation treatments

  • synthetic form of hirudin(leech saliva)
  • T1/2 ~25 min (3-4hrs with renal dysfunction)
  • IV only
  • less immunogenic than lepirudin (bc artificial)
  • Measured by aPTT or ECT
  • not common (newish/short half life
75
Q

Argatroban

  • T1/2
  • clearance?
  • immunogenic?
  • Measured/monitored by?
A

HIT, DTI anticoagulation treatment

  • MOST COMMON
  • T1/2 ~50min
  • clearance - hepatic
  • much less immunogenic (better for long term use)
  • Measured by aPTT or ECT
  • 50% lower incidence of hemorrhagic incidents than leech derived drugs
76
Q

Fondaparinux (Arixtra)

  • what
  • binds to
  • T1/2
  • clearance?
  • given?
  • Measured/monitored by?
A

HIT, Factor Xa Inhibitor, anticoagulant

  • a synthetic cousin of LMWH (but w/no heparin probs) does not directly inhibit thrombin
  • binds to ATIII
  • T1/2 ~ 20 hours
  • cleared unchanged by kidneys
  • SubQ only
  • Monitored by Anti-Xa assay or ACT
77
Q

Danaproid (orgaron)

  • what ?
  • available?
A

HIT, Factor Xa Inhibitor, anticoagulant

  • mixture of heparan sulfate, dermatan sulfate, and chondroitin sulfate
  • cross-reacts with HIT sera, so difficult to diagnosis
  • Not available in the US
78
Q

What to do when you have a HIT patient? (6)

A
  • Non-heparinized everything
  • monitor - ACT/ECT
  • NO stasis of blood
  • discontinue coagulation agent 20-30 min prior bc no reversal agent
  • MUF
  • recirculate with added agent and drain circuit asap
79
Q

ACT

A

whole blood clotting time accelerated bu using celite or kaolin activator (XII, XI)
normal value 92-128seconds

80
Q

ACT results can be artificially prolonged by what? (3)

A

hypothermia, hemodilution, and aprotinin (celite)

81
Q

aPTT

A
  • tests INTRINSIC coagulation pathway (VIII, IX, XI)
  • normal value - 26-39seconds
  • very sensitive to heparin, NOT useful during CPB
82
Q

PT

A

Tests Extrinsic Pathway VII
Normal value 10-14 seconds (lrg institutional variances)
-less sensitive to heparin than aPTT

83
Q

aPTT and PT how do they do test?

A

plasma is separated in citrated tube and spun to activate XII, known concen of …

aPTT- platelet phospholipid and Ca++ are added.
PT - tissue phospholipid and Ca++ are added

84
Q

Thrombin Time

A

Specific for measuring Common pathway
Normal value <17 seconds
sensitive to effects of heparin

85
Q

TT - how test works?

A

plasma isolated in citrated collection tube, Ca++ and concentration of thrombin are added to trigger clots
Lrg doses of thrombin convert this test to a measurement of Fibrinogen

86
Q 
Fibrin degradation (split) products
    - elevated levels can lead to?
A

Product of clot lysis

Elevated levels can lead to inhibition of fibrin monomer cross-linking and even induce platelet dysfunction

87
Q

TEG measures ? (5)

A

The efficiency of clot formation:

  • time takes for clotting to begin
  • speed of clot formation
  • clot strength
  • fibrinolysis
  • platelet function (platelet mapping)

Perf Tech II (exam 1) (9 decks)

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