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Pharmacology (MSK + Neuroscience) > Drugs for Numbness and Weakness 2 (Vascular Pathologies) > Flashcards

Drugs for Numbness and Weakness 2 (Vascular Pathologies) Flashcards

1
Q

What are the 2 kinds of vascular pathologies. State the names of the conditions treated.

A
  1. arterial - peripheral arterial disease
  2. venous - varicose veins + deep vein thrombosis
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2
Q

State the 4 classes of drugs used to treat peripheral arterial disease

A
  1. anti-hypertensives
  2. antilipid therapy
  3. antiplatelet therapy
  4. pentoxyfylline
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3
Q

What are the 7 common side effects of pentoxifylline?

A
  1. Gastrointestinal discomfort
  2. Belching
  3. Bloating
  4. Nausea
  5. Vomiting
  6. Dizziness
  7. Flushing
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4
Q

Whate are rare but potentially serious side effects of pentoxifylline?

A
  1. Angina
  2. Palpitations
  3. Bleeding
  4. Arrhythmias
  5. Anxiety
  6. Hallucinations
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5
Q

State the MOA of pentoxyfylline in peripheral arterial disease

A
  • non-selective PDE (phosphodiesterase) inhibitor that improves RBC deformability and reduces blood viscosity thus having haemorrheologic effect (improves blood flow)
  • methylated xanthine derivative
  • adenosine 2 antagonist
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6
Q

Name the drug used in antiplatelet therapy

A

ADP receptor blockers - clopidogrel

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7
Q

State the MOA of clopidogrel

A

ADP receptor blocker –> blocks P2Y12 recepotr –> prevents signalling pathways which prevent platelet activation and hence platelet aggregation

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8
Q

State the adverse effects of clopidogrel

A

Generally well tolerated

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9
Q

What is the benefit of ADP receptor blockers in IHD patients?

A

Reduction in the risk of atherothrombotic events in patients with IHD.

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10
Q

State the name of antilipid therapy used in peripheral arterial disease

A

HMG-CoA reductase - atorvastatin

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11
Q

State the MOA of atorvastatin in peripheral arterial disease

A
  1. inhibition of HMG reductase
  2. upregulates LDL-R on cell surface –> depletes extracellular cholesterol by increase number of specific cell surface LDL -R that can bind and internalise circulating LDL-C
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12
Q

State the adverse effects of atorvastatin in peripheral arterial disease

A
  • muscle - myopathy, rhabdomyolysis
  • liver - liver dysfunction
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13
Q

State the 2 drugs used as anti-hypertensives in peripheral arterial disease

A

ACE-inhibitors - captopril
ANGII Type 1 blocker - candesartan

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14
Q

State the MOA of captopril in peripheral arterial disease

A
  1. ACE-I inhibits conversion of ANGI to ANGII
  2. Decreased ANGII –> decreased vasoconstriction of SM –> decreased peripheral vascular resistance –> decreased BP
  3. Decreased ANGII –> decreased aldosterone secretion –> decreased Na+ and water retention –> increased urination –> decreased BP
  4. ACE-I also inhibits breakdown of bradykinin –> increased formation of NO and PG –> vasodilation –> decreased BP
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15
Q

State the adverse effecfts of captopril

A
  1. severe hypotension
  2. acute renal failure
  3. hyperkalaemia
  4. angioedema
  5. dry cough
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16
Q

In what situation should atorvastatin (antilipid) be used with caution

A
  1. pregnancy
  2. nursing mothers
  3. children or teens
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17
Q

State the MOA of candesartan in peripheral arterial disease

A
  1. ANGII type 1 blocker inhibits conversion of ANGI to ANGII
  2. Decreased ANGII –> decreased vasoconstriction of SM –> decreased peripheral vascular resistance –> decreased BP
  3. Decreased ANGII –> decreased aldosterone secretion –> decreased Na+ and water retention –> increased urination –> decreased BP
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18
Q

State the adverse effects of candesartan in peripheral arterial disease

A
  1. less dry cough
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19
Q

In what situation should candesartan (antihypertensive) be used with caution

A

pregnancy…

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20
Q

State the 2 classes of drugs used in treatment of varicose veins

A

varicose veins - engorged veins causing nerve compression

  1. mucopolysaccharide polysulphate –> treatment of inflamed, swollen varicose veins
  2. polidocanol –> treatment throguh sclerotherapy to narrow lumen of varicose veisn to force blood elsewhere
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21
Q

What is mucopolysaccharide polysulphate used for in varicose veins?

A

It is used to treat inflamed and swollen varicose veins due to its antithrombotic and anti-inflammatory properties.

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22
Q

What are the MOA of mucopolysaccharide polysulphate?

A
  1. Antithrombotic = Inhibits clotting factors by potentiating antithrombin activity
  2. Anti-inflammatory = Reduces capillary permeability and inflammatory mediators
  3. Improves Microcirculation = Promotes blood flow and tissue oxygenation
  4. Fibroblast Modulation = Enhances fibroblast activity and collagen synthesis, supporting wound healing
  5. Analgesic = Provides mild pain relief by modulating local inflammation.
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23
Q

State the adverse effects of mucopolysaccharide polysulfate

A

Local reaction
1. mild skin irritation (erythema, pruritus)
2. contact dermatitis with prolonged use

Systemic (rare)
1. hypersensitivity
2. systemic anticoagulation if used over large areas

24
Q

What is the mechanism of action of polidocanol?

A
  1. non-ionic surfactant that causes localized endothelial damage and induces clot formation leading to sclerosis and obliteration of the vein.
  2. mild anaesthetic - causes less pain and discomfort compared to other sclerostants
25
Q

What are potential adverse effects of polidocanol when used in sclerotherapy?

A

LOCAL
1. pain
2. redness
3. pruritus
4. hyperpigmentation
5. skin discolouration at the injection site

SYSTEMIC
1. allergic reaction (anaphylaxis)
2. n/v
3. headache

SERIOUS
1. thromboembolism
2. ulceration, or tissue necrosis if extravasation occurs

26
Q

What is the primary treatment approach for deep vein thrombosis (DVT)?

A
  1. anticoagulants such as rivaroxaban, apixaban, or low molecular weight heparin
  2. warfarin, dabigatran or edoxaban.
27
Q

What are common side effects of anticoagulants used for deep vein thrombosis (DVT)?

A
  1. bleeding
  2. bruising
  3. risk of haemorrhage
28
Q

State the MOA of anticoagulants.

A
  1. blocks activation of clotting fibres
  2. prevents conversion of fibrinogen to fibrin
  3. prevents polymerisation of fibrin to form meshwork to stabilise and hold thrombus together
29
Q

State the common oral anticoagulants used to treat DVT

A
  1. vitamin k antagonist - warfarin
  2. direct oral anticoagulant (DOAC) non-vitamin k antagonist - dabigatran, rivaroxaban
30
Q

State the common parenteral anticoagulants used to treat DVT

A
  1. heparin
  2. low molecular weight heparin derivatives - LMWHs - enoxaparin
  3. hirudins - lepirudin (NOT IMPORTANT)
31
Q

State the MOA of warfarin

A

Inhibition of vitamin K-dependent clotting factors (II, VII, IX, X) by inhibiting vitamin k reductase enzyme that reacivates oxidised vitamin k

32
Q

What is the reversal agent for warfarin?

A

vitamin k!!!!

33
Q

State the route of warfarin metabolism.

Can there be variability in response?

A

hepatic - primarily via CYP2C9

yes, variability occurs due to genetic polymorphisms in genes (CYP2C9 and VIt K Reductase Complex Subunit 1 - VKORC1)

34
Q

State 2 things we should monitor to titrate dose of warfarin

A
  1. international normalised ratio (INR)
  2. prothrombin time
35
Q

State the adverse effects of warfarin

A
  1. haemorrhage - bloody stool/urine, melena, excessive bruising, petechiae, persistent oozing from superficial injuries, excessive menstrual bleeding
  2. hepatitis (esp old dudes)
  3. cutaneous necrosis and infarction of breast, buttocks and extremities
36
Q

State the contraindications of warfarin

A
  1. hypersensitivity
  2. active bleeding, risk of pathologic bleeding after major surgery
  3. severe or malignant HTN
  4. severe renal/hepatic disease
  5. subacute bacterial endocarditis/pericarditis/pericardial effusion
  6. pregnancy

cautions
1. breast-feeding women
2. diverticulitis, colitis
3. mild htn
4. mild renal/hepatic disease
5. drainage tubes in orifices

37
Q

State some drugs and food that can interact with warfarin in DDI and DFI

A

INCREASE BLEED
- paracetamol long term therapy at high dose –> increase bleed
- allopurinol, NSAIDs, salicylates, PPI, metronidazole –> increase bleed
- traditional meds (gingko, reishi mushrooms, cranberry juice) –> increase bleed

DECREASE EFFICACY OF WARFARIN
- barbiturates, corticosteroids, spironolactone, thiazide diuretics –> decrease efficacy
- traditional meds (vitamin k, green tea) –> decrease efficacy

38
Q

What is the role of vitamin K in Warfarin therapy?

A

Vitamin K is necessary for the synthesis of clotting factors inhibited by Warfarin.

39
Q

What are the risks of combining NSAIDs with anticoagulants?

A

Increased risk of bleeding and gastrointestinal ulcers.

40
Q

State the common direct oral anticoagulants (DOAC) non-vitamin k antagonists

A
  1. dabigatran
  2. rivaroxaban
41
Q

State the MOA of dabigatran

A

dabigatran and its acyl glucuronide metabolites are** competitive reversible non-peptide antagonists of thrombin (factor IIa) **

dabigatran etexilate is the prodrug for dabigatran

42
Q

State the reversal agent of dabigatran.

State the MOA of the reversal agent.

State the clinical use of the reversal agent.

A

idarucizumab.

MOA: humanised monoclonal Ab fragment that binds dabigatran and its acyl glucuronide metabolites with higher affinity than the binding affinity of dabigatran to thrombin

Clinical use:
- reversal of anticoagulant effects of dabigatran in emergency surgery or life-threatening uncontrolled bleeding

43
Q

Explain why dabigatran etexilate must be administered in enteric coating preparations

A

Dabigatran extexilate has very low bioavailability of 3-7% hence enteric coating helps enhance absorption into bloodstream.

44
Q

State the MOA of rivaroxaban

A

rivaroxaban is a competitive reversible antagonist of activated factor X (Xa)

45
Q

State the reversal agent of rivaroxaban

A

andexanet alfa!

is a recombinant modified human factor Xa decoy protein

46
Q

Does dabigatran etexilate or rivaroxaban have faster reversibility of effects

A

rivaroxaban

the half life of dabigatran is 12-17 hours while that of rivaroxaban is a shorter 5-9 hours

47
Q

State the adverse effects of the DOAC (direct oral anticoagulants) non-vitamin k antagonists

A

dabigatran - GI, bleeding
rivaroxaban - bleeding

48
Q

State the common DDIs in the DOAC (direct oral anticoagulants) non-vitamin k antagonists

A

dabigatran
1. increase risk of bleeding - antiplatelets, anticoagulants, fibrinolytics, nsaids, ketocoonazole
2. reduced dabigatran level - rifampicin

rivaroxaban
1. increase risk of bleeding - antiplatelets, anticoagulants, nsaids, p-glyco-protein (P-gp), CYP3A4 inhibitors
2. reduced rivaroxaban level - P-gp, CYP3A4 inducers

49
Q

What is the function of Antithrombin III in anticoagulation?

A

It enhances the inactivation of thrombin and other coagulation enzymes.

50
Q

What is the advantage of low molecular weight heparins (LMWHs) over standard heparin?

A
  1. more predictable anticoagulant response
  2. lower risk of bleeding.
  3. longer half life (heparin = 1hr, lmwh = 4hr)
  4. higher bioavailability
51
Q

What are the indications for Antithrombin III administration?

A

Used in hereditary antithrombin deficiency and in certain cases of heparin resistance.

52
Q

State the MOA of heparin and LMWH (enoxaparin)

A

Heparin:
blocks surface contact triggered coagulation by potentiating action of ATIII and thereby inactivating thrombin
- binds tightly to ATIII and causes conformational change whcih exposes ATIII active site more for action by protease

LMWH (enoxaparin):
more selective in blockage of factor Xa and to a lesser extent thrombin (IIa)

53
Q

What are the side effects of using Heparin?

A
  1. bleeding (esp IV heparin)
  2. heparin-induced thrombocytopenia –> heparin binds to platelet factor 4 (PE4) on activated platelet surface –> IgG Ab against heparin-PE4 complex
  3. osteoporosis with long-term use.
  4. increased risk of epidural or spinal hematoma and paralysis in patients receiving epidural or spinal anaesthesia or spinal puncture
54
Q

State the contraindications of heparin and LMWH

A
  1. hypersensitivity
  2. active major bleeding
  3. thrombocytopenai or antiplatelet Ab

caution
1. elderly
2. risk of bleeding - prostethic heart valves, major surgery, regional or lumbar block anaesthesia, blood dyscrasis, recent birth, pericarditis, pericardial effusion, renal insufficiency (LMWH)

55
Q

State the DDI DHI and DFI of heparin and LMWH

A
  1. increase risk of bleeding with antiplatelets, anticoagulants, fibrinolytics, nsaids, ssri
  2. increase risk of bleeding with various food and herbs such as chamomile, fenugreek, garlic, ginger, gingko and ginseng
56
Q

State the reversal agent of heparin

A

protamine sulfate iv infusion

(incomplete reversal for LMWH)

57
Q

Can heparin and LMWH be used in pregnancy?

A

YES!
unlike warfarin, heparin and LMWH do not cross the placenta and have not been associated with fetal malformations

Pharmacology (MSK + Neuroscience) (8 decks)

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