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Hockerman Lectures Exam 4 Flashcards

1
Q

How does t-PA activate plasminogen?

A

It cleaves a arg-valine bond to create plasmin

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2
Q

What type of protein is t-PA?

A

Serine Protease

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3
Q

What 2 enzymes inhibit t-PA?

A

PAI-1 and PAI-2

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4
Q

What does aminocaproic acid inhibit?

A

The conversion of Plasminogen to Plasmin

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5
Q

What are the indications of Thrombolytic Therapy?

A

Acute MI (ASAP), Acute Ischemic Thrombotic Stroke (W/in 3hrs after excluding ICH), Pulmonary Embolism

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6
Q

What are the thrombolytic drugs?

A
  1. Alteplase 2. Reteplase 3. Tenecteplase
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7
Q

Which thrombolytic lacks the fibrin binding domain?

A

Reteplase

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8
Q

Which thrombolytic is more fibrin specific than t-PA?

A

Tenecteplase

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9
Q

Which thrombolytic is more potent and faster onset?

A

Reteplase

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10
Q

Which thrombolytic has a longer t1/2?

A

Tenecteplase

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11
Q

What is the underlying pathophysiology of the increase in t1/2 and enhanced activity of tenecteplase?

A

2 point mutations

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12
Q

When does streptokinase degrade a clot?

A

When it forms a 1:1 complex w/ plasminogen

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13
Q

All anti-fibrinolytics are derivatives of what?

A

Lysine; b/c plasmin binds to fibrin through a lysine binding site

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14
Q

How do antifibrinolytics work?

A

They are lysine analogs that bind to the receptor on plasminogen and plasmin

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15
Q

Which anti-fibrinolytic is more potent?

A

Tranexamic acid is 10X more potent than aminocaproic acid

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16
Q

Why is it difficult to break up clots that have formed post anti-fibrinolytic therapy?

A

The clots that form do not have plasminogen localized to the clot so the clot specific drugs (fibrin binding domains) don’t work as well on these clots

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17
Q

What induces the expression of Gp2b/3a receptors on plts?

A

ADP, 5-HT, and TXA2 when released from capsules

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18
Q

What cmpds released from plts are potent vasoconstrictors?

A

5-HT and TXA2

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19
Q

Which of the COX enzymes are more for inflammation?

A

COX2

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20
Q

When does hemostasis return to normal after ASA therapy abatement?

A

36 hrs

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21
Q

What ADP receptor is targeted by drugs?

A

P2Y12 - it is a Gi PRC that inhibits Adenylate Cyclase

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22
Q

What are the ADP receptor inhibitors?

A

Ticlopidine, Clopidogrel, Prasurgrel, and Ticagrelor

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23
Q

How do Ticlopidine and Clopidogrel Work?

A

They irreversibly block ADP receptor P2Y12 and prevent subsequent activation of Gp2b/3a

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24
Q

What is a risk of Ticlopidine?

A

TTP

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25
When do you use the thienopyridine class of ADP receptor inhibitors?
ACS, Acute MI, PVD, Coronary Stenting Procedures
26
How does Ticlopidine cause TTP?
It induces Abs against ADAMTS13
27
What is the reversible P2Y12 Inhibitor?
Ticagrelor; it binds to an allosteric site
28
What is special about Ticagrelor?
It does not require bioactivation and has a fast onset of action
29
How does prasugrel work?
It is metabolized by CYP3A4/2B6 to an active metabolite and forms an irreversible disulfide bond w/ the P2Y12 receptor
30
Why does clopidogrel have variable efficacy among pts?
It is activated by CYP2C19 and this enzyme has variable expression among pts.
31
Why does prasugrel have a more predicatble response than clopidogrel?
It is activated by CYP3A4/2B6 which has more predictable expression
32
What are the Gp2b/3A receptor Inhibitors?
Eptifibatide, Tirofiban, Abciximab
33
Why does Eptifibatide have a short duration of action?
It is a peptide and can be broken down (6-12hrs)
34
Which of the Gp2b/3a inhibitors are reversible?
Eptifibatide and Tirofiban
35
What is the half life of Tirofiban?
2 hours
36
What is the use of Tirofiban?
Combined w/ Heparin for tx of ACS
37
What is Abciximab?
Fab fragment of chimeric human/murine monoclonal Ab
38
Why does Abciximab have a inc. risk of bleeding?
Long duration of action
39
Uses of Abciximab?
Prevent thromboembolism in PCI and combined w/ t-PA for tx of acute MI
40
What are the phosphodiesterase inhibitors?
Dipyridamole and Cilostazol
41
What is the fxn of PDE inhibitors?
Inhibit plt. Aggregation
42
When do you use cilostazol?
Intermittent claudication
43
What are the Protease Activated Receptor Inhibitors?
Vorapaxar and Atopaxar (both in trials)
44
Why are PAR inhibitors important?
They prevent plts from being activated by thrombin
45
What are the 2 types of proteins for clotting factors?
Serine proteases and Glycoproteins
46
What are the glycoproteins?
They are the proteins used as cofactors for activation of proteases: 8,5,3, Protein S and to bind and inhibit thrombin Antithrombin III
47
Why is gamma-carboxylation important for coagulation?
Ca2+ can bind to the carboxylated residues and allow the cofactors to interact w/ the phospholipid membrane
48
Which isomer of Warfarin is the most potent?
S
49
What are all derivatives of Coumarin Anticoagulants?
Water soluble lactones
50
What Enzyme does coumarins inhibit?
Vit. K Epoxide Reductase which regenerates oxidized Vit. K back into its active form
51
Where is Warfarin Metabolized?
Liver CYP2C9 with variable expression
52
How can you counter Warfarin OD
Vit K in mild cases and FFP in severe cases
53
Why should you not use Warfarin in pregnancy?
It can freely pass through placenta and inc. risk of spontaneous abortion
54
What are the birth defects associated w/ Warfarin?
Nasal hypoplasia and abnormal bone formation
55
What is the fxn of antithrombin 3
Inactivates thrombin and 10a, (7a& 9a) to some extent
56
Which anticoagulant is effective immediately?
Heparin (and effect disapears quickly as well)
57
What is the antidote for heparin OD?
Protamine sulfate which binds heparin tightly and inactivates
58
How does Heparin induce TP in a pt?
Develops 7-12 days after therapy and abs form to platelet PF4-Heparin complex
59
What is the charged group on Heparin that interacts w/ antithrombin III
Sulfate Groups
60
Which heparins have the higher incidence of HIT?
Long-chain Heparins
61
What are the LMWH?
Dalteparin, Enoxaparin, and Tinzaparin
62
What are the benefits of LMWH over std Heparin?
Inc. bioavailability from SQ route, longer t1/5 = 4 hrs so less frequent dosing, and don't need to monitor clotting
63
How does the MOA of LMWH differ from Std Heparin?
It doesn't bind and inhibit thrombin as well
64
What is a benefit of Fondaparinux therapy?
t1/2 of 17-21 hrs
65
What are the orally available Factor 10a inhibitors?
Revaroxaban and Apixaban
66
MOA of Rivaroxaban and Apixaban?
Direct inhibition of active site of Factor 10
67
What are 2 risks of Rivaroxaban and Apixaban?
Need to reduce dose in renal impaired pts and inc. risk of stroke w/ discontinuation
68
What are the direct thrombin inhibitors?
Lepirudin, Desirudin, Bivalirudin, Argatroban, and Dabigatran
69
Why are Lepirudin and Desirudin so specific for direct inhibition of thrombin?
Bivalent binding to active site and exosite I
70
Which Direct thrombin inhibitors bind irreversibly to thrombin?
Lepirudin & Desirudin
71
Which direct thrombin inhibitors can induce a hypersensitivity rxn?
Lepirudin and Desirudin b/c they are proteins
72
What is the MOA of Bivalirudin?
It reversibly binds to the catalytic site and the exosite 1 of thrombin
73
What is the use of Bivalirudin?
PCI b/c it has a rapid onset and short duration
74
What is the clinical use of Argatroban?
HIT
75
Where does argatroban bind?
Reversibly to the active site of thrombin
76
Which direct thrombin inhibitor is a prodrug?
Dabigatran
77
What is ApoA1
Structural in HDL, produced in liver and intestine, mediates reverse cholesterol transport
78
What is ApoB-100?
Structural in VLDL, IDL, LDL
79
What is ApoB-48
Structural in Chylos and produced in the intestine
80
What is ApoE?
Ligand for LDL receptor remnant receptor; sequesters Chylos, IDL to liver
81
What is the key measurement in asseccing risk of CVD?
Ratio of Total Cholesterol to HDL-Cholesterol
82
What ratio of Total cholesterol to HDL-Cholesterol is assoc. w/ inc. CVD risk?
>4.5
83
What is the MOA of Bile acid binding Resins?
They inhibit reabsorption of Bile acid by exhanging Cl- for bile acid like a chromatography column, and they upregulate LDL receptors on the liver
84
What is cholestipol?
Bile acid binding resin
85
What is the MOA of Ezetimibe?
It inhibits cholesterol absorption from the intestines by inhibiting HPC1L1 transporter conformational change for clatherin internalization
86
How do Statins upregulatin hepatic LDL receptors?
They allow for SREBP and SCAP to be transported from the ER surface to the golgi where S1P and S2P can cleave the TF to go to nuc and upregulate
87
What statins are metabolized by CYP3A4
Lovastatin, Simvastatin, and Atorvastatin
88
What statins are metabolized by CYP2C9
Fluvastatin and Rosuvastatin
89
How is Pravastatin exreted?
Sulfation
90
Which stating is least likely to have drug-drug interactions?
Pravastatin
91
What is Juxtapid?
It inhibits assembly of ApoB containing Lipoproteins
92
What is the use of Juxtapid?
Familial Hypercholeterolemia - LDLR mutation
93
What is the MOA of mipomersen?
It hybridizes ApoB-100 mRNA in the liver for degredation; it is a phosphorothioate anti-sense oligonucleotide inhibitor
94
What fibrate must undergo bioactivation?
Fenofibrate to Fenofibric acid
95
What is the MOA of fibrates?
They bind to PPAR-_ and regulate gene transcription w/ retinoic acid receptor; this clears TGs from the blood
96
Why do you need to be careful using statins w fibrates?
Both cause rhabdo
97
What is an important drug interaction w/ fibrates?
Potentiate the action of Warfarin
98
What are the benefits of omega-3 FA intake?
They are used as substrates to produce TxA3 (less potent at stimulating plt aggregation) and PGI3 which is equipotent as prostacyclin
99
What is the MOA of Niacin?
Inc. lipase activity, dec hepatic VLDL production, inc HDL levels
100
What is a very effectivce drug for inc HDL levels
Niacin
101
How can you tx the flushing and itching assoc w/ Niacin?
Take a Cox inhibitor b/c mediated by prostaglandins
102
How does Niacin inhibit the breakdown of TG to FFA?
Activates GPR109a receptor

Pharm Exam 4 (3 decks)

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