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IPAP JUNIOR SEM. > PHARM II, BLOCK I > Flashcards

PHARM II, BLOCK I Flashcards

1
Q

What are the 5 steps of the pain process

A 
Transduction 
Conduction 
Transmission 
Modulation 
Perception
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2
Q

What is somatic pain

A

Nociceptive superficial pain

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3
Q

What is visceral pain

A

Nociceptive organ pain

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4
Q

What are the three types of chronic pains

A

Peripheral Nociceptive
Neuropathic
Centralized

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5
Q

What is the toxic metabolite of Tylenol

A

NAPQI

Damages the liver

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6
Q

What are the doses for Tylenol Toxicity

A

10-15 gm as a single dose is hepatotoxic

20-25 gm is pot. Fatal

Taking more than 4 gm in 24 hours is toxic

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7
Q

What is the antidote to Tylenol OD

A

N-acetyl cysteine

Acetadote/ Mucomyst

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8
Q

What is the MOA of ASA

A

Irreversibly inhibits COX-1 and COX-2 enzymes

Anti-platelet effect lasts for the life of the platelet (7 to 10 days)

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9
Q

Ketorolac can decrease opiod requirement by

A

25- 50 percent

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10
Q

What is the usage limit on ketorolac

A

No more than 5 days ( has a huge bleeding risk)

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11
Q

How does Ketorolac affect LnD

A

may adversely affect fetal circulation and inhibit uterine contractions

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12
Q

What NSAID has the lowest CV risk

A

Naproxen

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13
Q

Naproxen is FDA approved for what arthritic Dx

A

Gout

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14
Q

NSAID of use for gout attack

A

Indomethacin

Naproxen can also be used

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15
Q

What is the DOC for opthalmatic prep

Conjucntival inflammation and reduce pain after abrasions

A

Indomethacin

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16
Q

What is the 1st NSAID that showed accelerate closure of patent ductus arteriosus (PDA)

A

Indomethacin

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17
Q

What are the ADE and contra for Ibuprofen

A

ADE: GI irritation/bleeding (less frequent than with aspirin)
Low GI risk; moderate to high cardiovascular risk
Tinnitus

CONTRA: Angioedema
Aspirin sensitivity— bronchospasm

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18
Q

How does meloxicam interact with COX I and II

A

Preferentially inhibits COX-2 over COX-1 (at lower doses) looses selectivity at doses of 15mg/day

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19
Q

Clinical use of Meloxicam

A

OA and RA

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20
Q

What are the ADE for Diclofenac: an NSAID used to chronic MSK mild to moderate pain

A

High cardiovascular risk; moderate GI risk (oral formulation)
More frequently causes AST/ALT increase

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21
Q

What are the clin use of Celecoxib

A

OA and RA, Juvi RA, Ankylolsing and 1* dysmenorrhea

Developed to minimize ADE of GI
HIGH CV risk
And has a sulf group ( allergies)

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22
Q

Which NSAID has the least CV events

A

Naproxen

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23
Q

What drugs NSAIDS are the best for GI Bleeding Rsk pts

A

Celecoxib or non selective NSAIDS with a PPI or misoprostol

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24
Q

What are the three ways Opiods work

A
  • Inhibit the transmission of nociceptive input from the periphery to the spinal cord
  • Activate descending inhibitory pathways that modulate transmission in the spinal cord
  • Alter limbic system activity (pain perception
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25
Q

What are the 3 kinds of Opiod receptors

A

Mu

kappa

Delta

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26
Q

How do Mu(1) and Mu(2) receptors affect

A

μ1: analgesia

μ2: respiratory depression, miosis, reduced gastric motility, sedation, euphoria, pruritus, urinary retention, physical dependence

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27
Q

What receptors does morphine act on

A

Mu I and II ,

Weak affinity for delta and Kappa

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28
Q

Half life of morphine

A

2-4 hours

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29
Q

What is the metabolite of morphine

A

Hydromorphone

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30
Q

How often do we have to do REMS training to Rx hydromorphone

A

Every 2 years

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31
Q

What is Dilaudid

A

Hydromorphone

Metabolite of morphine
better oral absorption and more fat soluable

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32
Q

Is hydrocodone a partial or full agonist at the Mu receptor

A

Full ( pure)

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33
Q

Oxycodone is metabolized in to what two substances

A

Noroxycodone and oxymorphone

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34
Q

What is oxymorphone

A

Semi-synthetic Mu receptor agonist

Works way better than morphine

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35
Q

What is a prodrug that metabolizes into morphine

A

Codeine

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36
Q

What age group should codeine not be used in

A

Death Related to Ultra-Rapid Metabolism of Codeine to Morphine

  • Not recommended for <12 yo
  • Caution in 12-18 yo with asthma or other breathing problems
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37
Q

What receptors does Buprenorphine interact with

A

Mixed agonist/antagonist

Partial mμ receptor agonist and kappa receptor antagonist

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38
Q

What is the clin use for buprenorphine

A

Opiod detox

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39
Q

What receptors does butorphanol interact with

A

Partial agonist

Partial mμ and kappa receptor agonist

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40
Q

What partial agonist can be use in labor when an epidural is not possible

A

Butorphanol

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41
Q

What effects does Nalbuphine have on receptors

A

Mixed agonist/antagonist

Partial mμ receptor antagonist and strong kappa receptor agonist

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42
Q

What is meperidine

A

Demerol

Severe pain

Half life 15-30 hrs

Renally cleared

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43
Q

What patients CAN NOT receive meperidine

A

Renal or liver impairment or being too old
Heart conditions ( negative inotropy)
Pts on MAOI

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44
Q

How much stronger in fentanyl than morphine

A

75-125 times stronger

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45
Q

What is alfentanil

A

More rapid onset of fentanyl

Does not accumulate when infused

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46
Q

What is sufentanil

A

Slower onset version of fentanyl but last just as long

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47
Q

What is remifentanil

A

Fentanyl version that is infusion only
Rapid onset
Shortest duration of the fentanyl derivatives

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48
Q

What receptors does methadone act on

A

Potent agonist at mμ, kappa, and delta receptors
Antagonist at NMDA receptor
Inhibits serotonin and norepinephrine reuptake

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49
Q

What is the half life of methadone and what is the drug used for

A

Chronic pain syndrome: (neuropathic, cancer pain, and chronic non-cancer pain)
For opioid-tolerant patients only

Unpredictable t ½ 8-59hrs

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50
Q

What the difference between naloxone and naltrexone

A

Naloxone:

Shorter acting used for Opioid rescue
No systemic effect when given orally
Used orally for opioid induced constipation

Naltrexone:

Longer acting and slower onset
Used in opioid and alcohol addiction
100% absorbed and active orally

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51
Q

How often can naloxone be administered

A

Q 2-5 min

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52
Q

How does naltrexone work

A

Mμ receptor competitive antagonist

Competes but does not displace opioids

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53
Q

Naltrexone + Bupropion can treat what

A

Weight managment

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54
Q

How does tramadol effect SZR threshold

A

Lowers it

Abuse can cause SZR

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55
Q

What is considered opiod tolerant treatment/ exposure

A

More than 60 mg of MME/ day

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56
Q

How should Opiods be tapered

A

Taper by 20-50% per week (of original dose) for patients who are not addicted; the goal is to minimized adverse/withdrawal effects

Tapers slower than 10% per week (5-20% per month) better tolerated and appropriate for patients on long term opioids
Considered successful as long as patient is making progress

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57
Q

Oral morphine to IV morphine conversion

A

3:1

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58
Q

What does thrombin do

A

proteolytic enzyme that is formed from prothrombin that facilitates the clotting of blood by converting fibrinogen to fibrin

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59
Q

What are the three phases of thrombus formation

A

Adhesion, Activation, aggregation

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60
Q

In platelet homeostasis, what is the role of NO and prostaclyin

A

NO and prostacyclin induces cAMP synthesis.

cAMP decreases intracellular Ca2+ and inhibits GP IIb/IIIa activation

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61
Q

What is the receptor for Fibrin formation

A

GP IIb/IIIa

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62
Q

What factor mediates platelet adhesion

A

Von will factor

63
Q

What chemicals do adhered platelets release

A

Adhered platelets release numerous chemical mediators including Adenosine Diphosphate (ADP), Thromboxane A2 (TXA2), Serotonin (5HT), Platelet Activation Factor, etc.

64
Q

What is Arachidonic acid converted to by COX

A

Prostaglandin G2

65
Q

What is the role of 5HT IN PLATELET activation

A

Causes blood vessel to spasm, increase cytosolic calcium released
Results in narrowing the blood vessel, decreasing blood loss until clotting can occur
Serotonin release activates other platelets

66
Q

What is the “tissue factor” pathway

A

EXtrinsic pathway

Vit K dependent

Inhibited by warfarin which inhibits the hepatic synthesis of several clotting factors

67
Q

What is the “contact activation” pathway

A

INtrinsic pathway

inhibited by Heparin

68
Q

What does protein C do

A

Destroys activated factors Va and VIIIa

69
Q

What activates Prothrombin (II) into Thrombin (IIa)

A

Factor Xa

70
Q

What is protein S

A

Cofactor for protein C

71
Q

What does antithrombin III do

A

(inactivates IIa, VIIa, IXa, Xa): inhibits clotting factor proteases, especially thrombin, by forming complexes with them

72
Q

What test assesses the EXtrinsic pathway

A

Prothrombin Time (PT)

73
Q

What is the INR

A

standardized PT designed to account for differences in thromboplastin

74
Q

What lab test assesses the INtrinsic pathway

A

APTT

75
Q

Where does Warfarin inhibit the clotting cascade

A

Factors II, VII, IX and X

Inhibits vitamin K cofactors

Vitamin K epoxide reductase inhibition reduces available vitamin K needed by the Vit K dependent clotting factors: -factors II, VII, IX, and X as well as endogenous anticoagulant proteins C and S

76
Q

Warfarin blocks what vitamin reducatase?

A

Vitamin K ( V COR 1)

77
Q

Clinical use of Warfarin

A

Prophylaxis and treatment of DVT, PE, thromboembolic complications associated with A. fib and/or prosthetic cardiac valve replacement

Secondary prevention in the risk of death, recurrent MI, and thromboembolic events such as stroke or systemic embolization after MI

Protein C and S deficiency

78
Q

How many days does Warfarin take to go into effect

A

2-7 days

79
Q

What lab test monitors warfarin treatment

A

INR

80
Q

What is a normal INR range

A

0.8 and 1.2

81
Q

What is the INR goal for DVT prophylaxis and Tx of Thrombodic Dz

A

2-3

82
Q

What is the INR goal for artificial heart valves

A

2.3-3.5

83
Q

Purple Toe Syndrome is a ADE of what medication

A

Warfarin

84
Q

Can Warfarin be used in pregnancy

A

NO ! Cat X

85
Q

What enzyme metabolizes warfarin

A

CYP2C9

86
Q

What medication that increases GI bleeding should be avoided with Warfarin

A

NSAIDs

87
Q

What does a high INR mean

A

The pt takes longer to form a clot

88
Q

What are two PCC drugs

blood coagulation replacement products indicated for the urgent reversal of acquired coagulation factor deficiency

A

KCentra and Profilnine

Used to correct an active bleed

89
Q

If the INR is about 4.5 what is the Tx

A

Reduce or skip warfarin does,

Monitor the INR

90
Q

In the INR is 4.5 to 10 what is the Tx

A

Hold 1-2 doses of warfarin

Vit K can be used if urgent surgery is needed or bleeding risk is high

91
Q

If INR is greater than 10 what is the Tx

A

Hold warfarin and give vitamin K 2.5-5 mg
Monitor INR

Can give IV Vit K

92
Q

What is the Drug name for Vit K

A

Mephyton (PO) and Aquamephyton(IM)

Admin slow to avoid anaphylactic RXN

93
Q

What factors does heparin act on

A

Binds to antithrombin III and inhibits Xa and IIa

94
Q

Is heparin absorbed orally

A

No

95
Q

What is heparin induced thrombocytopenia

A

Hypercoag state from prolonged heparin exposure, causes a 50% decrease in platelets

96
Q

What are the ADE of heparin

A

Bleeding, HIT, Osteoporosis and Hyperkalemia

97
Q

What is a normal aPTT time

A

28-38 seconds

98
Q

An aPTT above 70 indicates..

A

An aPTT above 70 indicates..

99
Q

What is the preferred anticoagulant in pregnancy

A

LMWH

100
Q

What is Protamine sulfate

A

Reversal drug for heparin

101
Q

What is the boxed warning on LMWH

A

Spinal and epidural hematomas

102
Q

Does LMWH need to be monitored

A

No

103
Q

What is the DOC for anti coagulation in cancer pts

A

Dalteparin

104
Q

How does Fondaparinux effect the clotting cascade

A

Blinds to antithrombin III and selectively inhibits Factor Xa

(More specific LMWH)

105
Q

When Tx acute DVT with fondaparinux what drug must be used in combination

A

Warfarin

106
Q

Does protamine sulfate completely reveres LMWH

A

NO

107
Q

What are the Three LMWH

A

Fondaparinux
(most specific to Xa)
Enoxaparin
Dalteparin (Cancer)

108
Q

What are the Three Direct Factor Xa Inhibitors

A

Rivaroxaban
Apixaban
Edoxaban

109
Q

Can warfarin be used in pts with prosthetic valves

A

YES ( one advantage of Warfarin)

110
Q

What factors does heparin act on

A

Binds to antithrombin III and inhibits Xa and IIa

111
Q

Is heparin absorbed orally

A

NO

112
Q

What is heparin induced thrombocytopenia

A

Hypercoag state from prolonged heparin exposure, causes a 50% decrease in platelets

113
Q

What are the ADE of heparin

A

Bleeding, HIT, Osteoporosis and Hyperkalemia

114
Q

An aPTT above 70 indicates..

A

28-38 seconds

115
Q

An aPTT above 70 indicates..

A

May indicate internal bleeding

116
Q

What is the preferred anticoagulant in pregnancy

A

LWMH

117
Q

When can Edoxaban be used in DVT/ PE Tx

A

After 5 days of Tx with a parenteral anticoagulant

118
Q

What are Rivaroxaban and Apixaban used for

A

Stroke prevention and systemic embolism in patients with non-valvular atrial fibrillation
Prophylaxis of DVT following hip or knee surgery
DVT/PE treatment

119
Q

What is andexxa

A

(Antidote for Direct Factor Xa inhibitors)

Recombinant Factor Xa

120
Q

What is the safest direct factor Xa medication for pregnancy

A

Apixaban

121
Q

What are the warnings for Direct Factor Xa inhibitors

A

Avoid in pts with liver problems ( Riva and Apixaban)

or hepatic impairment ( Edoxaban)

122
Q

What is the allergy precaution for Protamine sulfate

A

Fish allergy

123
Q

What class is Bivalirudin and Argatroban

A

Direct thrombin inhibitors

124
Q

What is the drugs to use in PCI

A

Direct Thrombin inhibitors

Bivalirudin and Argatroban

125
Q

How is Bivalirudin cleared

A

Renal

126
Q

How is argatroban cleared

A

By the liver

127
Q

What two labs are monitored with Bivalirudin and argatroban

A 
APTT (1.5-2.5 baseline) 
and ACT ( >2.5 times baseline)
128
Q

What is Dabigatran

A

Direct thrombin inhibitor prodrug metabolized by P-glycoprotein

129
Q

What drug must be stopped for 2 hours prior to taking dabigatran

A

Antacids

130
Q

When converting a pt from Warfarin to Dabigatran what must the INR be

A

Below 2.0

131
Q

What is the antibody for Dabigatran

A

humanized monoclonal antibody fragment that binds to dabigatran and its metabolites with higher affinity then the binding affinity of dabigatran to thrombin, neutralizes anticoagulant effect

ONLY USED in EMERGENCY

132
Q

What is the antidote for Unfiltered Heparin

A

Protamine sulfate

133
Q

What is the Antidote for LMWH

A

None really, may consider protamine sulfate

134
Q

What is the antidote for Warfarin

A

Phytonadione ( VIT K )

May consider PCC > FFP

(Prothrombin complex concentrate)

135
Q

What is the antidote for Dabigatran

A

Idarcuzimab

136
Q

What is the reversal/ antidote for Rivaroxaban, Apixaban, and Edoxaban

A

Recombinant Factor Xa ( Andexxa)

137
Q

What monitoring is required for LMWH

A

None

138
Q

What is the MOA of fibrinolytics

A

dissolve clots by activating the conversion of plasminogen to plasmin that hydrolyzes (cleaves) fibrin, lysing thrombus

139
Q

What is the time frame for best Fibrinolytic Tx

A

Within 3 hours

some benefit at 12

140
Q

Clinical use of fibrinolytics

A

Life threatening events

STEMI
STROKE
PE
Severe DVT

141
Q

What is the black box warning for ticagrelor

A

Black Box Warning: decreased effectiveness with aspirin doses greater than 100 mg

142
Q

How does Clopidogrel and prasugrel work compared to ticagrelor

A

Clopidogrel and Prasugrel:

Irreversibly inhibits the binding of adenosine diphosphate (ADP) to its P2Y12 receptor
Resulting in inhibition of the GPIIb/IIIa receptors required for platelet aggregation

Both are PRODRUGS

Ticagrelor:

Reversibly inhibits the binding of ADP to its P2Y12 receptor
Resulting in inhibition of the GPIIb/IIIa receptors required for platelet aggregation

143
Q

For a non pci capable hospital what is the Tx approach to STEMI

A

MONA then

Transfer to a PCI hospital within 120 min

Or

Fibrinolytics within 30 min
(Tenecteplase, Reteplase, or alteplase)

Then

Clopidogrel

Then

Heparin or enoxaprin or Fondaparinux

144
Q

For a PCI capable hospital what is the Tx approach to STEMI

A 
MONA 
Then P2Y12 ( Clopidogrel, Ticagrelor)

And/or
GPIIb/IIIa Antagonist
(Tirofiban High Dose Bolus, Eptifibatide Double Dose)

Or

Bivalirudin

With or without heparin

145
Q

In the absences of contras, what is the medical managment for all patients with a NSTEMI

A

aspirin (ASA) + P2Y12 receptor inhibitor +/- glycoprotein IIb/IIIa inhibitors

( Clopidogrel, and Eptifibatide)

146
Q

What the clearance for Abciximab vs Eptifibatide and Tirofiban

A

Abciximab does not require renal adjustment

Eptifibatide and Tirofiban does

147
Q

What is the role of GPIIb/IIIa inhibitors

A

Abciximab: Adjunct to PCI for the prevention of cardiac ischemic complications in patients undergoing PCI
In patients with unstable angina not responding to conventional medical therapy when PCI is planned within 24hrs

Eptifibatide and Tirofiban:
Administered with heparin and aspirin in ACS and PCI to reduce thrombotic cardiac events

148
Q

What are the absolute contra for fibrinolytics

A 
History of intracranial hemorrhage
History of cerebrovascular lesion
Known intracranial neoplasm
Ischemic stroke ≤ 3 months
Aortic dissection
History of head or facial trauma within 3 months
Active bleeding / bleeding diathesis
149
Q

What are the three GPIIb/IIIa inhibitors

A

Abciximab (monoclonal Ab)
(High risk of causing RXN)

Eptifibatide
Tirofiban

150
Q

What drugs must be administered with TPA

A

Asparin and heparin

151
Q

TPA drugs alteplase is approved for?

Reteplase and tenecteplase approved for?

A

Alteplase: STEMI, PE, Ischemic stroke w/in 3 hours, and catheter clearance

Reteplase and tenecteplase are only approved for acute STEMI

152
Q

What is the MOA of TPA ( Alteplase, ect)

A

activate plasminogen that is bound to fibrin in a thrombus, thereby initiating fibrinolysis

153
Q

What is the MOA of Urokinase

A

THROMBOLYTIC ENZYME

human enzyme synthesized by the kidney that directly converts uncomplexed plasminogen to active plasmin, degrades fibrin and clotting factors V and VII

(UNCOMPLEXED!! UNBOUND)

IPAP JUNIOR SEM. (43 decks)

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