Pharmacology: Anticoagulants, Chemotherapyantibiotics Flashcards

1
Q

Ancrod is a defibrinogenating agent derived from venom. What is it not recommended for use?

A

Associated with severe bleeding

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2
Q

Antifungal are targeted to fungal cell wall. Name some. What can these cause?

A

Amphotericin B, flucytosine, fluconozole, itraconazole, metronidazole, voriconazole; can case nephrotoxicity

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3
Q

Bacterial cell wall inhibitors are used to treat gram negative bugs.

A
  1. Vancomycin
  2. Monolactum
  3. Cabapenam
  4. Penicillins, cephalosporins, bacitracin
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4
Q

Can you give Heparin for Type I or Type II?

A

onCPB for Type 1

For type 2, only if they haven’t received heparin in the last 90 days

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5
Q

Can you give platelets for Type II?

A

No

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6
Q

DNA inhibitors block DNA gyrase and DNA synthesis. Name some

A

Quinolones, fluroquinolones, metronidazole

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7
Q

DO NOT USE _______ with a topical irrigation of antibiotics, collagen implants, etc…

A

Cell saver

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8
Q

The dose of DTI is adjusted by achieving a _______ of ______

A
  1. PTT; 60-80 secds or

2. a PTT of 1.5-2.5x the pts baseline aPTT

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9
Q

Fibrinolytics and thrombolytics are used to treat what?

A

Acute MI or PE

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10
Q

Fibrinolytics and thrombolytics convert ______ to ______, enhancing fibrolyisis

A

Plasminogen, plasmin

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11
Q

Give some examples of Glycoproteins IIb/IIIa? When should you stop use B4SX?

A
  1. Abciximab (Reopro): 72 hours
  2. Eptifibatide (Integrillin): 24 hours
  3. Tirofiban (Aggrastat): 24 Hour
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12
Q

Give some examples of gram negative bacteria

A

S. aureus (skin), S. epidermis (surgery wounds, indwelling catheters), Group A beta hemolytic streptococus (strep throat, rheumatic fever)

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13
Q

Glucagon ______ glucose levels and insulin _____ glucose level. (increase or decrease)

A

Increases, decreases

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14
Q

Glycoproteins ______ the fibrinogen/ GB IIb/IIIa receptor

A

antagonizes

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15
Q

Glycoproteins IIb/IIIa inhibitors are used to prevent platelet _____ and ______ formation?

A

Aggregation, thrombus

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16
Q

These Hirudins have the highest affinity for _____ and work by inhibiting ______ of protein C.

A

Thrombin, thrombin activation

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17
Q

How common is HIT?

A

3% of Sx

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18
Q

How does Glucagon help Tx hypoglycemia?

A
  1. It promotes glycogenolysis & glyconeogenesis

2. Also can be used in heart failure due to excessive beta blockage

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19
Q

How does Protamine reverse Heparin?

A

It neutralizes it by combing to heparin to form an inert salt

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20
Q

How does warfarin work?

A

An anticoagulant; it’s a vitamin K antagonic that causes reduction of synthesis of factors: 2, 7, 9, 10

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21
Q

How fast should you give protamine?

A

1mg/kg or 20 mg per 60 second period

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22
Q

How is Argatroban eliminated?

A

hepatic

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23
Q

How many days should a patient stop using Clopidogrel (plavix) before surgery? Tricildopine?

A
  1. 7 days

2. 4 days

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24
Q

How much will 1 unit of insulin decrease glucose by?

A

25-30mg/dL

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25
Q

How soon should you stop Heparin before surgery?

A

6 hours

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26
Q

How would you reverse DTIs?

A

Wait for the half life, then ultrafiltrate (45-69% amt removed vai UF)
Give recombinant FVIIa

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27
Q

How would you treat Heparin resistance?

A
  1. FFP= 2-4 units in adults

2. ATIII conc = 1000U dose will increase ATIII levels 30 % in adults: this is = to 4-5 units of FFP

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28
Q

How would you treat Warfarin use or Vitamin K deficiency?

A

Give FFP (15ml/kg) to treat INR>1

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29
Q

Is Amicar (EACA) or Cyclokapron (TXA) a more potent antifibrinolytic?

A

Cyclokaptron by 10x

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30
Q

Is LMWH used in Cardiac Sx?

A

No, it is poorly neutralized and has an incomplete reversal with protamine

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31
Q

Is the half life for LMWH longer or shorter than regular heparin?

A

longer 4-5 hours

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32
Q

Name the 3 most common antifibrinolytics

A
  1. Amicar
  2. Txa
  3. DDAVP
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33
Q

NPH and regular insulin, which one is short acting?

A

Regular insulin

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34
Q

On a TEG what does alpha measure?

A

the speed to reach a solid clot; it is decreased by thrombocytopenia

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35
Q

Platelet activation is caused by what?

A

Thromboxane A2 and ADP activation of platelets causes PLT activation. becomes “sticky”

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36
Q

Protein synthesis inhibitors bind to ribosomal 30/50 subunit inhibiting normal translation of bacterial proteins. Name some.

A
  1. tetracycline, doxycycline
  2. aminoglycosides, gentamycin, streptomycin
  3. macrolides- erythromycin, azithromycin
  4. lincosamides- clindamycin
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37
Q

What 2 drugs can cause cardiac toxicity?

A

Cyclophosphamide & Doxorubicin

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38
Q

What are antifibrinolytics used for?

A

Enhance postoperative hemostasis by binding to plasmin and plasminogen preventing degradation of fibrin to FSP

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39
Q

What are DTI? What do they do?

A
  1. Direct thrombin inhibitors

2. bind to the active site of thrombin for the use of pts with HIT

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40
Q

What are Hirudins?

A

Hirudin is a compound made by medicinal leeches that interferes with the body’s ability to form blood clots. Such anticoagulation invovles the inhibition of the protein thrombin, which catalyzes blood clot formation

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41
Q

What are some antibiotic protein synthesis inhibitors?

A

Tetracycline, doxycycline, clindamycine -> things that end in (-cyclin)

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42
Q

What are some antibiotic DNA inhibitors?

A

Qunolones, fluroquinolones, metronidiazole

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43
Q

What are some fibrinolytics and thrombolytics?

A
  1. streptokinase
  2. urokinase
  3. tPA
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44
Q

What are the acquired ATIII deficiency?

A
  1. decreased synthesis from liver cirrhosis
  2. drug induced
  3. increased excretion
  4. accelereated consumption
  5. dilutional
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45
Q

What are the drugs to give for antifungal?

A

Amphotericin B, flucytocin, fluconozole, itraconazole, metronidazole, voriconzole

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46
Q

What are the extrinsic pathway factors?

A

7, 3

47
Q

What are the factors in the common pathway?

A

1, 2, 5, 10

48
Q

What are the inherited ATIII deficiency?

A
  1. 1 in every 2000 to 20000 people, autosomal dominant

2. levels are

49
Q

What are the intrinsic pathway factors?

A

12, 11, 9, 8

50
Q

What are the various factors involves in the clotting cascade?

A
I- Fibrinogen
II. Prothrombin
III. Tissue factor (Thromboplastin)
IV. Calcium
V. proaccelerlin (Labile)
VII. Proconvertin (stable)
VIII. ANF (antihemophilic)
IX. Christmas Factor (plasma thromboplastin component)
X. Stuart-Prower
XI. Plasma Thromboplastin
XII. Hageman Factor
XIII. Fibrin Stabilizing Factor
51
Q

What are the various Hirudins

A
  1. Desirudin/Lepirudin
  2. Bivalrudin (angiomax)
  3. Argatroban
52
Q

What are the Vitamin K dependent factors?

A

2, 5, 7, 9, 10

53
Q

What can you give to help Tx hypoglycemia?

A

Glucagon

54
Q

What can you reverse the effects of ASA with?

A

You can’t!! Effects stay with through the lift of the platelet

55
Q

What common pathogens are we concerned with the most? Why?

A
  1. Gram negative (S. aureus/skin)
    S. epidermis (surg. wounds, indwelling catheters) Group A beta hemolytic stretpcoccus (strep throat, rheumatic fever)
  2. Gram positive: E. Coli (GI), Shigella, Salmonella, Klebsiella, H. influenza, Neisseri, Pseudomonas, Nosocomial infections
56
Q

What do NSAIDS inhibit? For how long?

A
  1. Inhibit tXA2 (THromboxane A2)

2. for 24-48 hours

57
Q

What does ASA ihibit? For how long? Used to treat what?

A
  1. Blocks Cox-1 and Cox-2 enzyme activity which inhibits TXA2 synthesis and ADP release by platelets
  2. 9-12 days (life of platelet)
  3. Used to treat stroke, acute MI
58
Q

What does Clopidogrel (Placix) and Ticlidopine do to platelets?

A

Cause inhibition of ADP released by platelets

59
Q

What does DDAVP increase?

A

The release of factor VIIIC and vWF THUS increasing platelet adhesiveness

60
Q

What does dexamathasone do?

A

PRevents SIRS and cerebral edema; preserves lung f(x) during CPB, controls rejection post transplant

61
Q

What does Dipyridomole (persantine) inhibit? When should patient stop taking drug before surgery?

A
  1. Inhibit Adenosine

2. 24 hours

62
Q

What does Heparin bind to?

A

ATIII

63
Q

What does insulin do?

A

Promotes glucose and K+ entry into cells

64
Q

What does NPH do?

A

Protamine helps delay insulin absorption and prolongs its effects

65
Q

What does solu-cortef do?

A

Inhibit cytokine production

66
Q

What does solu-medrol do?

A

Inhibit leukocyte chemotaxis; increases the stress response in kidneys

67
Q

What does the MA measure on a TEG?

A

platelet function; the clot strength, the dynamic properties of fibrin and platelet bonding

68
Q

What drug blocks platelet activation by ADP?

A
  1. Clopidogel (plavix); Ticlidopine
  2. NSAIDs (ASA, ibuprofen, naproxen)
  3. ASA
69
Q

What factors are affected by the PT?

A

Factor 7 (extrinsic) and common factors (1, 2, 5, 10)

70
Q

What is an infection w/ mix of gram - and gram + pathogens that’s usually encased in an abscess wall? Give some examples?

A
  1. Anaerobe
  2. Bacteriodes fagalis
  3. Dificile C. Botulinum C Tetani
71
Q

What is considered to be physiological heparin concentration that we all aim for?

A

3-4 units/ mL per blood circulating volume

72
Q

What is considered to be triple therapy for heart transplant patients?

A

Cyclosprine, Azathioprine, Corticosteroids

73
Q

What is heparin resistance?

A

The inability to achieve ACT >400 sec despite heparin doses >600 u/kg

74
Q

What is highly absorbable in plastic?

A

Insulin; this is why we don’t give this on pump

75
Q

What is HIT Type I?

A

Mild degree of thrombocytopenia resulting from heparin therapy; onset is 2-5 days

76
Q

What is HIT Type II?

A

IgG-mediated antibodies recognize platelet factor 4 heparin complexes on platelets surface; causes activation of platelets, monocytes

Rirsk for DIC

Antibodies level drop w/n 4-8 weeks onset is 5-10

77
Q

What is hypoglycemia associated with?

A

Increased morbidity

78
Q

Why is LY30?

A

Meausres the % of lysis 30 mins after the MA is reached

79
Q

What is PT and the normal value for it?

A

Prothrombin Time; 9-15 secs

80
Q

What is PTT?

A

Partial Thromboplastin time; 22-36 secds

81
Q

What is so different about LMWH?

A

It is poorly neutralized and has an incomplete reversal with Protamine

82
Q

What is the Gold Standard for HITT assays?

A

Heparin Induced serotonin release assay

83
Q

What is the intermediate acting Corticosteroids?

A

Solu-medrol

84
Q

What is the long acting Corticosteroids?

A

Dexamethasone

85
Q

What is the major elimination method of Bivalrudin?

A

80% proteolysis, renal 20%; half life 25 min

86
Q

What is the NaCHO3 formula?

A
  1. (BE x wt (kg))/ 4

2. Give half of the calculated dose

87
Q

What is the ratio of Heparin to protamine?

A

1: 1.3 for every 100 u heparin

88
Q

What is the short acting Corticosteroids?

A

Solu-cortef

89
Q

What is Warfarin?

A

Coumadin (warfarin sodium) is an anticoagulant that acts by inhibiting vitamin K- dependent coagulation factors

90
Q

What other drug is Dipyridamole administered along with? Persantine is used to treat what? In what kind of patients?

A
  1. Warfarin
  2. PVD
  3. pts with stents or prosthetic valves
91
Q

What pathogen stain weakly gram + and are responsible for TB and leprosy? What would you treat it with?

A
  1. Mycobacteria

2. Isoniazid rifampin, streptomycin

92
Q

What pathways are reflected by ACT (activated clotting time)? What drugs affects ACT?

A
  1. Intrinsic and common

2. Heparin therapy, DTI

93
Q

What pathway does Heparin affect?

A

The instrinsic and common; affects factors 9, 10, 11, 12 and plasmin

94
Q

What pathways does Warfarin affect?

A

Extrinsic and common

95
Q

What tests would indicate Warfarin use or Vitamin K deficiences?

A
  1. prolonged PT or INR goal 2-3
  2. Normal to mildly prolonged PTT
  3. Bleeding time and platelet count is unaffected
96
Q

What type of affinity binding quality does Bivalrudin (Angiomax) have for thrombin?

A

Intermediate

97
Q

What type of drugs are cell wall inhibitors?

A

Vancomycin, monolactum, cebapenam, penicillins, cephalosporins, bacitracin

98
Q

What type of pathogen are sensitive bacterial cell wall inhibitors?

A

Gram (-) bacteria

99
Q

What will happen if you give Protamine too fact?

A

Histamine release causing systemic Hypotension

100
Q

What would you give to help tx hyperglycemia?

A

NPH and regular insulin

101
Q

What yeast-form produces spores/budding? Sites and treatment?

A
  1. Fungus (Candida)
  2. Mouth (thrush) = nystatin
  3. Brain = fluconazole, flucytosine
  4. Vaginitis = miconazole, metronidazole
  5. Systemic = amphotericn B, fluconazole, itraconazole
102
Q

What is it most beneficial to give antifibrinolytics?

A

Before CPB and maintained throughout

103
Q

When might patients be on cyclophosphamide and Doxorubicin drugs?

A

If they are getting limb perfusion

104
Q

When should you stop argatroban?

A

4-6 hours before surgery

105
Q

When should you stop Bivalrudin (angiomax)?

A

2-3 hours before Sx

106
Q

When should you stop LMWH?

A

12-24 hours before Sx

107
Q

When should you stop Warfarin?

A

2-4 days before Sx

108
Q

When would you stop Hirudins (desirudin/lepirudin)?

A

8 hours before Surgery

109
Q

Which Hirudins has the lowest affinity for thrombin? Should you use it on CPB?

A

Argatroban; NO (not currently approved yet)

110
Q

Who would have a Heparin allergy?

A

DM patients that take NPH have fish allergies, have been previously exposed to Heparin or those who have had a vasectomy

111
Q

Why are topical irrigation beneficial?

A
  1. High sustained cone, at site of infections
  2. Limited potential for systemic absorption & toxicity
  3. Reduced volumes of antibodies use
  4. Less potential for development of antibiotic resistance
112
Q

Why cant you give Hirudins to renal failure patients?

A

Because it is eliminated by renals

113
Q

Why is Cyclokaptron more potent?

A

Because it has a greater affinity to plasminogen than EACA

114
Q

Why is hyperglycemia bad?

A

Because it can contribute to neuro dysfunction and impair wound healing